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C681  .C83  Diseases  of  the  I 


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Digitized  by  the  Internet  Arciiive 

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http://www.archive.org/details/diseasesofheartOOcowa 


DISEASES   OF  THE   HEART 


DISEASES    OF   THE 
HEART 


BY 

JOHN    COWAN,    D.Sc,    M.D.,   F.R.F.P.S. 

PROFESSOR   OF    MEDICINE,    ANDEKSOn's    COLLEGE   JTEDICAL   SCHOOL  ; 

PHYSICIAN.    ROYAL    INFIRMARY  ;     LECTURER    IN    CLINICAL 

MEDICINE      IN      THE      UNIVERSITY,      GLASGOW  ; 

EXAMINER   IN   MEDICINE,    ROYAL   ARMY 

MEDICAL   COLLEGE 


WITH  CHAPTERS  ON 

THE  ELECTRO-CARDIOGRAPH 

By  W.  T.  RITCHIE,  M.D.,  F.R.C.P. 

PHYSICIAN,    DEACONESS   HOSPITAL  ;    ASSISTANT   PHYSICIAN,    ROYAL 
INFIRMARY,    EDINBURGH 

AND 

THE  OCULAR  MANIFESTATIONS  IN 
ARTERIOSCLEROSIS 

By  ARTHUR  J.  BALLANTYNE,  M.D.,  F.R.F.P  S. 

SURGEON,    EYE    INFIRMARY,    GLASGOW 


LEA    &    FEBIGER 

PHILADELPHIA    AND    NEW    YORK 
1914 


VY-a-<r 


>\1 


_   2-i^J 


TO    THE    MEMORY    OF 

THE   OLD 
GLASGOW  HOYAL   INFIRMARY 

1794—1912 

WHICH    WAS    SBEVED    IN    THEIR    GENERATION 

BY 

EGBERT  COWAN 

(1769— ISOS) 

EGBERT  COWAN 

(1796—1841) 

SOlIETIilE   PROFESSOR   OF  MEDICAL   JURISPRUDENCE 
IN   THE   UNIVERSITY   OF   GLASGOW 

■JOHN  BLACK  COWAN 

(1S29— 189C) 

SOMETIME   PROFESSOR   OF   MATERIA  MEDIC  A 
IN  THE   UNIVERSITY   0¥   GLASGOW 

AND 

JOHN  COWAN 


® 


PREFACE 

During  the  last  ten  years  great  advances  have  been  made  in 
our  knowledge  of  the  diseases  of  the  heart  and  arteries.  Xew 
methods  of  histological  technique  have  revealed  lesions  which 
were  hitherto  unappreciated,  and  experimental  research  has 
deciphered  their  causes.  The  sphygmomanometer,  the  poly- 
graph, the  electro-cardiograph,  and  the  Eontgen  rays,  have 
become  accessible  to  the  chnician,  and  the  data  thus  acquired 
have  elucidated  some  of  the  many  problems  which  awaited 
solution;  while  the  pharmacologists  have  defined  the  uses  of 
such  drugs  as  digitalis  more  accurately  than  had  been  pre- 
viously possible. 

The  following  pages  are  an  attempt  to  review  the  whole 
subject  in  the  Hght  of  these  recent  advances,  and  to  present 
to  the  practitioner  the  results  which  have  been  attained,  and 
their  bearing  upon  the  practical  work  of  diagnosis,  'prognosis, 
and  treatment.  They  are  based  in  the  main  upon  my  personal 
experience  and  the  records  in  my  own  wards,  though  I  have 
utihzed,  where  it  seemed  desirable,  the  numerous  monographs 
and  articles  which  have  recently  appeared,  and  the  experience 
of  my  medical  friends. 

The  importance  of  the  cardiac  muscle  in  the  maintenance  of 
the  circulation  renders  necessary  a  short  account  of  the  diseases 
by  which  it  is  affected.  Arterial  disease  and  its  influence  upon 
the  heart  are  discussed  in  the  three  succeeding  chapters.  The 
myogenic  theory  and  the  various  disturbances  of  cardiac 
function  are  considered  at  some  length,  and  are  accompanied 
by  an  account  of  the  electro-cardiograph.  Acute  endocar- 
ditis, chronic  valvular  disease,  myocardial  weakness,  and  peri- 
carditis then  follow  in  order. 

The  chapters  so  kindly  contributed  by  W.  T.  Eitchie  ("  The 


viii  PREFACE 

Electro-Cardiograph"),  and  A.  J.BaUantyne("The  Ocular  Mani- 
festations in  Arterio-Sclerosis  ")  are  of  special  value,  as  they  are 
written  by  recognized  authorities  upon  these  particular  subjects. 

The  illustrations  are  mainly  original,  and  I  must  express 
my  indebtedness  to  the  kindness  of  Professors  Arthur  Keith, 
Robert  Muir,  and  J.  H.  Teacher  for  their  permission  to  utihze 
the  specimens  in  their  museums.  The  former  has  also  allowed 
me  to  reproduce  three  of  his  diagrams.  The  microscopic  pic- 
tures have  been  made  from  my  own  collections  and  those  of 
A.  M.  Kennedy  and  A.  W.  Harrington.  The  skiagrams  were 
taken  from  my  patients  by  J.  E.  Eiddell. 

The  polygraph  tracings  are,  with  one  exception,  from  my 
own  collection.  This  I  have  done  purposely,  even  in  cases 
where  more  perfect  examples  might  have  been  obtained  else- 
where, in  order  to  show  the  frequency  with  which  disturbances 
of  cardiac  function  occur  in  the  ward  work  of  a  general  hospital, 
and  the  possibiHty  of  recording  them  in  a  busy  clinique.  Several 
of  them  were  obtained — ^unaided — by  my  residents. 

I  have  not  attempted  to  supply  a  full  bibliography,  and  the 
references  which  are  given  refer  to  statements  which  may  not 
yet  be  generally  accepted  or  known,  or  add  point  to  the  text. 
My  own  papers  will  be  found  to  contain  numerous  references 
to  their  particular  subject.  I  have  made  little  reference  to 
standard  works,  but  I  must  acknowledge  my  indebtedness  to 
the  writings  of  G.  W.  Balfour,  Sir  W.  Broadbent,  A.  E.  Cushny, 
G.  A.  Gibson,  W.  H.  Gaskell,  H.  Huchard,  James  Mackenzie, 
A.  E.  Sansom,  W.  Stokes,  and  Graham  Steell;  and  to  the 
articles  in  Sir  Clifford  AUbutt's  and  in  Sir  William  Osier's 
"  Systems." 

I  have  great  pleasure  in  acknowledging  the  kind  assistance 
in  my  task  of  many  friends,  in  particular  Robert  Muir,  and  my 
collaborators  and  colleagues,  W.  T.  Ritchie,  Archibald  W. 
Harrington,  A.  M.  Kennedy,  J.  R.  C.  Greenlees,  David 
MacDonald,  and  G.  B.  Fleming;  my  past  and  present  residents, 
without  whose  willing  aid  my  records  must  of  necessity  have 
been  scanty;  and  last,  but  not  least,  Farquhar  Macrae. 

J.  C. 


CONTENTS 

CHAPTEK  I 
THE  DISEASES  OF  THE  MYOCARDIUM 

Pages 

The  myocardium.  Tlie  coronary  circulation.  Tlie  muscle  cells. 
Hypertrophy.  Atrophy.  Ischsemic  atrophy.  Granular  de- 
generation. Hyaline  degeneration.  Dissociation.  Fatty  infil- 
tration. Fatty  degeneration.  Fibrosis.  Infarct  and  para- 
arterial  fibrosis.  Peri-arterial  fibrosis.  Syphilis.  Aneurism  of 
the  heart.     Rupture  of  the  heart  ...  -  1-29 


CHAPTER  II 

THE  DISEASES  OF  THE  ARTERIES 

The  arteries.  Arteriosclerosis.  The  lesions.  Etiology.  High 
blood-pressure.  Chronic  renal  disease.  Increased  viscosity  of 
the  blood.  Polycythaemia  hypertonica.  Plethora.  The  infec- 
tions. Focal  lesions.  Atheroma.  Mes-arteritis.  Endarteritis 
obliterans.     Medial  calcification.     Etiology        -  -  30—: 


CHAPTER  III 

THE  SYMPTOMS  OF  ARTERIAL  DISEASE 

High  blood-pressure.  Cardiac  hypertrophy.  Consecutive  mitral 
disease.  UrseiTiic  symptoms.  Emphysema.  Dyspnoea.  Cere- 
bral symptoms     ------  54-71 


CHAPTER  IV 
By  A.  J.  Ballantyne 

THE  OCULAR  MANIFESTATIONS  IN  ARTERIO- SCLEROSIS 

72-74 


PAOKS 


X  CONTENTS 

CHAPTER  V 

THE  TREATMENT  OF  ARTERIO-SCLEROSIS 

Vaso-ililators.    Elimination.    Digitalis.    Caffeine.   Theobromine.   The 

treatment  of  high  blood-pressure.     Diet.     Exercise  -        75-97 

CHAPTER  VI 

THE  MYOGENIC  THEORY 

The   myogenic   theory.     The  primitive  tissue  of  the  heart.     The 

polygraph.     The  interpretation  of  cervical  curves     -  -      98-113 

CHAPTER  VII 

By  W.  T.  Ritchie 

THE  ELECTRO-CARDIOGRAPH 

The  interpretation  of  electro-cardiograms  -  -  -     1 14-122 

CHAPTER  VIII 

.    STBIULUS  PRODUCTION 
Infantile  irregularities      ...--.     123-124 

CHAPTER  IX 

EXCITABILITY 

Tiie  extra-systole.     Ventricular,  auricular,  and  nodal  extra-systoles. 

The  significance  of  extra-systoles     -  -  -  -    125-132 

CHAPTER  X 

NODAL  RHYTHM 

Nodal  rhythm:   (1)  paroxysmal;  (2)  continuous.     The  relationship 

of  the  cardiac  valves  and  the  a-v  tissues.     Myocarditis        -     133-158 

CHAPTER  XI 

CONTRACTILITY 

Pulsus  altcrnaus.     The  significance  of  pulsus  alternans  -  -    159-161 


CONTENTS  xi 

CHAPTER  XI 1 
CONDUCTIVITY 

PAGES 

Heart-block:  full;  partial.  Irregularities  of  the  pulse  duo  to  de- 
fective conduction.  The  Stokes-Adams  syndrome.  1'he  auricular 
contractions  in  heart-block.  Nervous  causes  of  heart-block. 
Prognosis.     Treatment  ....  -    162-173 

CHAPTER  XIII 

TONICITY 
Dilatation  of  the  heart    -  -  -  -  -  -  174 

CHAPTER  XIV 

COUPLED  RHYTHMS 

Coupled  rhythm:  in  heart-block;  in  auricular  fibrillation;  from 
extra-systoles;  in  nodal  rhythm.  The  significance  of  coupled 
rhythms         -...---    175-18! 

CHAPTER  XV 

PAROXYSMAL  TACHYCARDIA 

The  nodal  form.  Etiology.  Symptoms.  Prognosis.  Treatment. 
The  relationship  of  paroxysmal  tachycardia  and  auricular 
flatter  .  .  -     •        -  -  -  -    184 -I!)? 

CHAPTER  XVI 

AURICULAR  FLUTTER 

The  cervical  curves.  The  arterial  curves.  Nervous  causes.  Symp- 
toms.    Prognosis.     Treatment.     The  action  of  digitalis      -     198-210 

CHAPTER  XVII 

AURICULAR  FIBRILLATION 

The  pulsus  irregularis  perpetuus.  Etiology.  The  cervical  curves. 
The  arterial  curves.  Valvular  murmurs  in  auricular  fibrillation. 
Prognosis.     Treatment  .  .  .  -  -    211-219 

CHAPTER  XVIII 

ACUTE  ENDOCARDITIS 

The   lesions.     Etiology.     Acute   rheumatism    and   chorea.     Simple 

and  malignant  cases.     Blood  cultures  -  -  -    220-233 


xii  CONTENTS 

CHAPTER  XIX 
ACUTE  ENDOCARDITIS 


PAGES 


The  symptomg.  Latent  endocarditis.  Valvular  murmurp.  The 
pulse.  Subcutaneous  nodules  and  cutaneous  manifestations. 
Embolism.  Fever.  Cardiac,  cerebral,  pulmonary,  and  general 
symptoms      -  -  -      .       -  -  -  -    234-250 

CHAPTER  XX 

ACUTE  ENDOCARDITIS— Con^wwed 

Diagnosis.     Prognosis.     Treatment.     Rest.     Salicylates.    Vaccines. 

Sera.     General 251-260 


CHAPTER  XXI 

CHRONIC  VALVULAR  DISEASE 
The  lesions.     Etiology.     The  causes  of  aortic  and  mitral  disease    201-281 

CHAPTER  XXII 

THE  SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE 

The  symptoms  of  chronic  valvular  disease.  The  causes  of  symptoms. 
Dyspnoea.  Cheyne- Stokes  breathing.  Paroxysmal  dyspnoea. 
Cough.  Cardiac  discomfort  and  pain.  Palpitation.  (Edema. 
Gastro  -  intestinal  symptoms.  Cerebral  symptoms.  The 
symptoms  of  mitral  and  aortic  disease        -  -  -    282  -30S 

CHAPTER  XXIII 

MYOCARDIAL  FAILURE  WITHOUT  VALVULAR  DISEASE 

Myocardial  failure  fin  the  infections;  in  myocardial  disease         -     309-319 

CHAPTER  XXIV 

THE  DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE 

The  significance  of  physical  signs.  Epigastric  pulsation.  The  causes 
of  murmurs.  The  physical  signs  of  myocardial  weakness  in  the 
infections.  Mitral  valvular  disease.  Aortic  valvular  disease. 
Pulmonary  valvular  disease.  Tricuspid  valvular  disease.  Con- 
genital heart  disease.  The  Bruit  de  Roger.  Patent  ductus 
arteriosus       -------    320--360 


CONTENTS  xiii 

CHAPTER  XXV 
THE  PROGNOSIS  IN  CHRONIC  CARDIAC  FAILURE 

PAGES 

The  nature  of  the  lesion.  The  site  of  the  lesion.  The  grade  of 
the  lesion.  The  rhythm  of  the  heart.  The  influence  of  con- 
current disease.  The  degree  of  compensation.  The  cause  of 
failure.     Age.     Sex.     Social  circumstances  -  -  -    361-369 

CHAPTER  XXVI 

THE  TREATMENT  OF  CHRONIC  CARDIAC^FAILURE 

Work.      Nutrition.      The     treatment     of     symptoms.      Digitalis. 

Caffeine,  etc.     General  .....    370-384 

CHAPTER  XXVII 

ACUTE  PERICARDITIS 

The  lesions.  Etiology.  The  infections.  Intrathoracic  disease. 
Pyaemia.  Terminal  pericarditis.  The  symptoms.  The  effects 
of  effusion.  The  physical  signs.  Latent  pericarditis.  Prog- 
nosis -....-.-    385-402 

CHAPTER  XXVni 

ADHERENT  PERICARDIUM 

Indurative  mediastino-pericarditis.  Pericarditis  interna  el  externa. 
Etiology.  The  symptoms.  Pick's  disease.  The  signs  of  ad- 
herent pericardium    ....--    403-418 

PNEUMO-PERICARDIUM 

Etiology.     The  physical  signs.     Prognosis  -  -  -    418-425 

CHAPTER  XXIX 

THE  TREATMENT  OF  PERICARDITIS 

The  treatment  of  dry  pericarditis;  of  pericarditis  with  effusion;  of 

adherent  pericardium.     Operative  procedures  -  -    426-429 

Index     ----_-._  431 


LIST  OF  ILLUSTRATIO^S 


COLOURED  PLATES 

FIG.  PAGE 

8.  Fibrosis  of  the  Anterior  Wall  op  the  Left  Ventricle      -    facing      16 
11.  Marked    Narrowing    of    the    Orifices    of   the   Coronary 
Arteries   from   Syphilitic  Disease  of  the  Aorta:    In- 
farct of  Heart  -  -  -  -  -  -  ,,  18 

44.  Right  Fundus  Oculi  prom  a  Case  op  Chronic  Nephritis 

(A.  J.  Ballantyne)    ----..,,  74 


IN  THE  TEXT 

1.  Diagram  of  Arterial  Circulation  of  Normal  Heart         -  -  3 

2.  Diagram  of  Arterial  Circulation  in  a  Heart  where  the  Left 

Coronary  Artery  was  obstructed              ....  6 

3.  Diagram  of  Arterial  Circulation  in  a  Heart  where  the  Right 

Coronary  Artery  was  obstructed             -            -  •          -  -  7 

4.  Ischemic  Atrophy  op  Muscle               -            -            -            -  -  8 

5.  Granular  Degeneration  of  Muscle  -  -  -  -  -  9 
G.  Fatty  Degeneration  op  Muscle:  Patchy  Form  -  -  -  12 
7.  Fatty  Degeneration  of  Muscle:  Difpuse  Form  -  -  -  13 
9.  Dystrophic  Fibrosis  of  Wall  op  Left  Ventricle   -             -  -  17 

10.  Para-arterial  Fibrosis              -            -            -            -            -  -  18 

12.  Peri-artbrlal  Fibrosis  -            -            -            -            -            -  -  19 

13.  Interstitial  Myocarditis          -            -            -            -            -  -  20 

14.  Perifascicular  Fibrosis             -            -            -            -            -  -  21 

15.  Interstitial  Myocarditis:  Focal  Form  (A.  M.  Kennedy)  -  -  22 

16.  Interstitial  Myocarditis:  Difpuse  Form  (A.  M.  Kennedy)  -  23 

17.  Gumma  op  Heart            -            -            -            -            -            -  -  25 

18.  Syphilitic  Myocarditis              -            -            -            -            -  -  27 

19.  Infarct  of  Papillary  Muscle,  with  Rupture           -            -  -  27 

20.  Arterio-Sclerosis:  Intimal  Thickening          -             -            -  -  33 

21.  Arterio-Sclerosis:  Medial  Fibrosis    -            -            -            -  -  34 

22.  Arterio-Sclerosis:  Medial  Fibrosis    -             -             -            -  -  35 

XV 


xvi  LIST  OF  ILLUSTRATIONS 

Firi.  PAGE 

23.  Blood-Pressure  Chart:  Large  White  Kidney          -             -  -  36 

24.  Blood-Pressure  Chart:  Small  White  Kidney           -             -  -  37 

25.  Early  Atheroma             -            -            -            -            -            -  -  42 

26.  Syphilitic  Mesaortitis  -            -            -            -            -            -  -  43 

27.  Syphilitic  Mesaortitis  -             -             -             -             -             -  -  44 

28.  Syphilitic  Mesaortitis  -            -            -            -            -            -  -  45 

29.  Syphilitic  Mesaortitis  -            -            -            -            -            -  -  45 

30.  Endarteritis  Obliterans           -            -            -            -            -  -  46 

31.  Endarteritis  Obliterans:  Syphilitic  Form  (A.  W.  Harrington)  -  47 

32.  Skiagram:  Medial  Calcification  (J.  R.  Riddell)      -             -  -  48 

33.  Blood-Pressure  Tracing:  Aortic  Regurgitation     -            -  -  58 

34.  Blood-Pressure  Tracing:  Chronic  Nephritis            -            -  -  59 

35.  Sphygmogram:  Aortic  Regurgitation-            -            -            -  -  01 

36.  Blood-Pressure  Chart:  Chronic  Nephritis  -            -            -  -  62 

37.  Blood-Pressure  Chart:  Aortic  Valvular  Disease  -            -  -  62 

38.  Blood-Pressure  Chart:  Pneumonia    -             -             -             -  -  63 

39.  Blood-Pressure  Chart:  Mitral  Disease        -            -            -  -  63 

40.  Blood-Pressure  Chart:  Chronic  Nephritis  -            -            -  -  64 

41.  Blood-Pressure  Chart:  Mitral  Disease        -            -            -  -  66 

42.  Blood-Pressure  Chaut:  Mitral  Disease;  Cirrhotic  Kidney  -  67 

43.  Blood-Pressure  Chart:  Chronic  Nephritis   -            -            -  -  68 

45.  Blood -Pressure  Chart:  Chronic  Nephritis  -            -            -  -  77 

46.  Blood -Pressure  Chart:  Bronchitis     -            -            -            -  -  78 

47.  Blood-Pressure  Chart:  Mitral  Disease;  Cirrhotic  Kidney  -  80 

48.  Blood-Pressure  Chart:  Cirrhotic  Kidney    -            -            -  -  80 

49.  Blood-Pressure  Chart:  Bronchitis     -             -             -    .        -  -  83 

50.  Blood-Pressure  Chart:  Bronchitis     -             -            -             -  -  85 

51.  Blood-Pressure  Chart:  Hemiplegia    -            -            -            -  -  86 

52.  Blood -Pressure  Chart:  Chronic  Nephritis  -            -            -  -  Sg 

53.  Blood-Pressure  Chart:  Chronic  Nephritis  -            -            -  -  89 

54.  Blood-Pressure  Chart:  Mitral  Disease;  Cirrhotic  Kidney  -  90 

55.  Heart  of  Ox,  dissected  to  show  the  a. v.  Bundle  (A.  Keith)  -  100 

56.  Human  Heart,   dissected  to  show  the   a.v.  Node   and  Bundle 

(A.  Keith)         ........  101 

57.  Heart  oe  Walrus,  dissected  to  show  the  a. v.  Bundle  (A.  Keith)  -  102 

58.  The  Sino-Auricular  Node  (A.  M.  Kennedy)             -            -  -  103 

59.  Curves  prom  Brachial  Artery,  Right  Neck,  and  Apex-Impulse  -  106 

60.  Curves  from  Brachial  Artery,  Right  Neck,  and  Apex-Impulse  -  107 

61.  Curves  from  Brachial  Artery,  Second  Left  Intercostal  Space, 

AND  Apex-Impulse       -------  108 

62.  Diagram   showing    Surface    Relations    of   Carotid   Artery    and 

Jugular  Vein  (A.  Keith)     ------  109 

63.  Curves  from  Right  Neck  and  Apex-Impulse            -            -  -  113 

64.  Electro-Cardiogram:  Normal  (W.  T.  Ritchie)          -            -  -  116 


LIST  OF  ILLUSTRATIONS  xvii 

"Q-  PAGE 

65.  Electko-Cardiogbam  and  Cervical  Curves  (W.  T.  Ritchie)          -  117 

66.  Electro-Cardiograms  from  Cases  of  Mitral  Stenosis  and  Aortic 

Regurgitation  (W.  T.  Ritchie)                   ....  ng 

67.  Electro-Cardiogram:  Partial  Heart-Block  (W.  T.  Ritchie)        -  119 

68.  Electro-Cardiograjm:  Full  Heart-Block  (W.  T.  Ritchie)             -  120 

69.  Electro-Cardiogram:  Ventricular  Extra-Systoles  (W.  T.  Ritchie)  120 

70.  Electro-Cardiogram:  Auricular  Flutter  (W.  T.  Ritchie)            -  121 

71.  Electro-Cardiogram:  Auricular  Fibrillation  (W.  T.  Ritchie)      -  121 

72.  Curves  of  Radial  Pulse  and  Respiratory  Movements     -  facing  123 

73.  Blood-Pressure  Tracing,  showing  Extra-Systole              -       ,,  123 

74.  Curves  showing  Interpolated  Ventricular  Extra-Systole     ,,  123 

75.  Curves  showing  Ventricular  Extra-Systole          -            -      ,,  123 

76.  Curves  showing  Ventricular  Extra-Systole          -            -            -  126 

77.  Curves  showing  Ventricular  Extra-Systole,  followed  by  Auric- 

ular Extra-Systole              -             -             -             -             -             -  126 

78.  Curves  showing  Auricular  Extra-Systole  -            -            -            .  127 

79.  Curves  showing  Nodal  Extra-Systole         ....  ^28 

80.  Curves  of  Brachial  Artery  and  Apex-Impulse;  Auricular  Fib- 

rillation       ........  129 

81.  Curves  showing  Nodal  Extra-Systole         ....  130 

82.  Curves  showing  Nodal  Rhythm         .....  135 

83.  Curves  showing  Nodal  Rhythm        .            .            .            .            .  133 

84.  Curves  showing  Nodal  Rhythm        .....  142 

85.  Curves  showing  Nodal  Rhythm         .....  145 

86.  Curves  showing  Nodal  Rhythm        .....  148 

87.  The  a. v.  Node  and  Bundle  (A.  M.  Kennedy)        -            -            -  152 

88.  Longitudinal  Section  of  the  Heart            -            -   "         -            -  153 

89.  Transverse  Section  of  the  Heart  -            -            -            -            -  154 

90.  Transverse  Section  of  the  Heart  -            -            -            -            -  155 

91.  The  a. v.  Node  and  Bundle:  Mitral  Disease  (A.  M.  Kennedy)     -  156 

92.  The  a. v.  Node  and  Bundle:  Mitral  and  Aortic  Disease  (A.  M. 

Kennedy)       ........  156 

93.  The  a. v.  Node  and  Bundle:  Mitral  and  Tricuspid  Disease  (A.  M. 

Kennedy)        ........  157 

94.  Curves  showing  Pulsus  Alternans  succeeding  an  Extra-Systole  160 

95.  Curves  showing  Pulsus  Alternans  -            -            -            -            .  160 

96.  Curves  showing  Pulsus  Alternans  -            -            -            -            -  160 

97.  Curves  showing  Pulsus  Paradoxus  -----  160 

98.  Curves  showing  Full  Heart-Block  -            -            -            -            -  163 

99.  Curve  of  Apex-Impulse  showing  Full  Heart-Block          -  facing  164 

100.  Curves  showing  Partial  Heart-Block          -             -             -       ,,  164 

101.  Curves  showing  Partial  Heart-Block         -            -            -      ,,  164 

102.  Brachial  Pulse  in  Full  Heart-Block         -            -            -      ,,  169 

103.  Curves  in  Coupled  Rhythai  due  to  Extra-Systoles         -            -  176 


xviii  LIST  OF  ILLUSTRATIONS 

FIO.  PACK 

104.  Curves  in  Cotjpled  Rhythm  dtte  to  Pabtial  Heakt-Block           -  177 

105.  CUKVES      SHOWING      VENTRICULAR      ExTRA-SySTOLES,      FOLLOWED      BY 

AuRicuLAB  Extra-Systoles             -            -            -            -            -  178 

106.  Curves  in  Partial  Heart-Block        .....  178 

107.  Curves  in  Fuxl  Heart-Block  (W.  T.  Ritchie)        -            -            -  180 

108.  Curves  of  Brachial  Artery  and  Apex-Impulse:  Auricular  Fib- 

rillation       .-..----  181 

109.  Brachial  Curve  showing  the  Effects  of  Pressure  upon  the  Left 

Vagus  Nerve             .......  181 

110.  Curves  in  Coupled  Rhythm:  Xodal  Rhythm           .             .            -  182 

111.  Curves  from  Brachial  Artery.  Right  Neck,  and  Apex-Impulse; 

Paroxysmal  Tachycardia   ------  187 

112.  Curves  sho\ving  Varying  Sinus  Rhythm      -            -            -  facing  192 

113.  Curves  showing  Varying  Sinus  Rhythm      -            -            -      .,  192 

114.  Curves  from  Brachial  Artery,  Right  Neck,  and  Apex- 

Impulse  IN  Paroxysmal  Tachycardia,  showing  Change 

OF  Rhythm     -             -             -             -             -             -             -       ,,     -  192 

115.  Curves  in  Paroxysmal  Tachycardia             ....  193 

116.  Electro-Cardiograju;  Auricular  Flutter  (W.  T.  Ritchie)            -  199 

117.  Curves  in  Auriculak  Flutter  (5  to  1  Ratio)         -            -            -  200 

118.  Curves  in  Auricular  Flutter  (4  to  1  Ratio)         ...  20O 

119.  Curves  in  Auricular  Flutter  (2  to  1  Ratio)         -            -            -  201 

120.  Curves  in  Auricular  Flutter  (Varying  a.  v.  Ratio)          -   facing  202 

121.  Brachial  Curve:  Auricular  Flutter            -             -             -       ,,  202 

122.  Curves  in  Auricular  Flutter            -             -             -             -       ,,  202 

123.  Brachial  Curve:  Auricular  Flutter            .             .             .             .  202 

124.  The  Radial  Pulse  in  Auricular  Fibrillation        -             -             -  212 

125.  Curves  in  Auricular  Fibrillation    -            -            -            -            -  213 

126.  Curves  in  Auricular  Fibrillation    -----  214 

127.  Acute  Verrucose  Endocarditis         -            -            -            -            -  221 

128.  Malignant  (Pneumococcic)  Endocarditis      -            .            .            .  223 

129.  Malignant  Endocarditis,  Infecth^e  Aortitis          -            -            -  224 

130.  Malignant  (Pneumococcic)  Endocarditis      .            -            .            .  225 

131.  Malignant  (Streptococcic)  Endocarditis     ....  226 

132.  Chart  showing  Rise  of  Pulse-Rate  on  Cessation  of  Sodium  Sali- 

cylate            ........  235 

133.  Curves  showing  Nodal  Rhythm         .....  242 

134.  Curves  showing  Nodal  Rhythm         .             .             .             .             .  248 

135.  Chart  of  a  Case  of  Malignant  Endocarditis         -            -            -  252 

136.  Chaut  showing  Subnormal  Wave  of  "Pyrexia"  -            -            -  253 

137.  Calcareous  Infiltration  of  Aortic  Valve  -            -            -            -  262 

138.  Chronic  Mitral  and  Tricuspid  Stenosis      -            -            -            .  263 

139.  Chronic  Mitral  Endocarditis             -            .             .             .             .  264 

140.  Aortic  Incompetence   .......  265 


LIST  OF  ILLUSTRATIONS  xix 

FIG.  PAGE 

141.  Cheonic  Mitral  and  Atjeiculae  Endocarditis         .  .  .  266 

142.  Syphilitic  Disease  of  Aortic  and  Mitral  Valves  -  -  268 

143.  Chronic  Renal  Disease:  Patchy  Thickening  of  Mitral  Cusps     -  272 

144.  Chronic  Renal  Disease:  Diffiise  Thickening  of  Mitral  Cusps     -  273 

145.  Chronic   Renal   Disease:    Diffuse    Thickening    of   Aortic   and 

Mitral  Cusps  .......  274 

146.  Brachial  and  Respiratory  Curves  in  Cheyne-Stokes  Breathing 

facing  287 

147.  Blood-Pressure  Tracing:  Aortic  Regurgitation   -  -  -  300 

148.  DlAGRAJil  SHO\VING   SURFACE   RELATIONS   OF   THE   LuNGS,    HeART,    AND 

Cardiac  Valves  (A.  Keith)  -  -  -  -  -  321 

149.  Diagram  shoaving  Surface  Relations  of  the  Pericardium,  Heart, 

AND  Great  Vessels  (A.  Keith)       .....  322 

150.  Curves  showing  "  In-verted  "  Apex-Impulse  -  -  -  323 

151.  Curves  of  Epigastric  Pulsation  due  to  Aoria      -  -  -  323 

152.  Curves  of  Epigastric  Pulsation  due  to  Right  Ventricle  -  323 

153.  Curves  of  Epigastric  Pulsation  due  to  Left  Ventricle     -  -  324 

154.  Curves  from  Brachial  Artery,  Second  Left  Intercostal  Space, 

AND  Apex -Impulse     .......  324 

155.  Curves  from  Fourth  Right  Intercostal  Space  and  Apex-Impulse  324 

156.  Diagraji  showing  Surface  Relations  of  Heart  and  Lungs         -  325 

157.  DiAGRAii  showing  Area  of  Cardiac  Dulness  -  -  -  326 

158.  Diagram  showing  Time  Relations  of  the  Cardiac  Contractions, 

THE  Cardiac  Sounds,  and  the  Valvular  Murmurs         -  -  328 

159.  Skiagram:  Hypertrophy  of  Left  Ventricle  (J.  R.  Riddell)       -  334 

160.  Diagram  showing  Area  of  Cardiac  Dulness  in  Mitral  Stenosis  -  335 

161.  Diagram  showing  Distribution  of  Presystolic  Murmur  -  -  337 

162.  Skiagram:  Hypertrophy  of  Right  Ventricle  (J.  R.  Riddell)     -  338 

163.  Diagram  showing  Area  of  Reduplicated  Second  Sound  -  -  340 

164.  Diagram  showing  Area  of  Early  Diastolic  Mitral  Murmur      -  340 

165.  Blood-Pressure  Chart:  Mitral  Disease       -  .  .  .  341 

166.  Blood-Pressure  Chart:  Mitral  Disease;  Cirrhotic  Kidney         -  342 

167.  Diagram  showing  Area  of  Cardiac  Dulness  in  a  Dilated  Heart  343 

168.  Diagram  showing  Area  of  Cardiac  Dulness  in  Mitral  Reflux    -  343 

169.  Diagram  showing  Distribution  op  Murmur  in  Mitral  Reflux      -  344 

170.  Diagram  showing  Distribution  of  Murmur  in  Mitral  Reflux      -  344 

171.  Diagram  showing  Distribution  of  Murmur  in  Aortic  Stenosis     -  348 

172.  Diagram  showing  Distribution  of  Murmur  in  Aortic  Stenosis     -  348 

173.  Diagram  showing  Area  of  Cardiac  Dulness  in  Aortic  Reflux     -  349 

174.  Diagram  showing  Distribution  of  Murmur  in  Aortic  Reflux      -  350 

175.  Diagram  showing  Distribution  of  Murmur  in  Aortic  Reflux      -  350 

176.  Sphygmogram:  Aortic  Reflux  .....  351 

177.  Diagram  showing  Distribution  of  Murmur  in  Pulmonary  Stenosis  355 

1 78.  Diagram  showing  Distribution  of  ]\1urmur  in  Pulmonary  Reflux  -  355 


XX  LIST  OF  ILLUSTRATIONS 


PAGE 


179.  Diagram  SHOWING  Distribution  OF  Murmur  IN  Tkicuspid  Reflux    -  357 

ISO.  Diagram  showing  Distribution  of  Murmur  in  Tricuspid  Stenosis  -  357 

181.  Diagram  showing  Distribution  of  Murmur  in  Patent  Ductus 

Arteriosus      ...-----  358 

182.  Stenosis  of  Left  Pulmonary  Artery  by  a  Secondary  Malignant 

Growth  ....---.  359 

183.  Diagram  showing  Distribution  of  Murmur  in  Stenosis  of  Left 

Pulmonary  Artery  ......  360 

184.  Diagram  showing  Distribution  of  Murmur  in  Stenosis  op  Left 

Pulmonary  Artery  ......  360 

185.  Chart  of  Pulse-Rate  and  Urinary  Output,  showing  the  Influence 

of  Rest  ........  371 

186.  Chart  op  Pulse-Rate,  showing  the  Influence  of  Digitalis        -  382 

187.  Diagram  of  Area  of  Dulness  in  Pericarditis        -  -  -  399 

188.  Diagram  of  Area  of  Cardiac  Dulness  of  a  Dilated  Heart       -  400 

189.  Skiagram:    Pericarditis    with    Effusion;    Left    Pneumothorax 

(J.   R.   RiDDELL)  -  -  -  -  -  -  -  401 

190.  Curves  showing  Systolic  Retraction  of  Apex-Impulse    -  -  407 

191.  Curves  showing  Broadbent's  Sign    -  .  -  .  .  408 

192.  Curves  showing  Systolic  Retraction  op  Fourth  Right  Inter- 

space ---------  408 

193.  Curves  showing  Pulsus  Paradoxus  ....  -  409 

194.  Curves  showing  Systolic  Retraction  op  Lower  End  of  Sternum  414 

195.  Skiagram:  Mediastino-Pericarditis  (J.  R.  Riddell)  -  -  417 

196.  Diagram  of  the  Physical  Signs  in  a  Case  of  Pneumo-Pericardium  421 

197.  Diagram  of  the  Physical  Si3ns  in  a  Case  of  Pneumo-Pericardium  422 

198.  Skiagram:  Pneumo-Pericardium  (J.  R.  Riddell)     -  -  -  423 

199.  Skiagram:  Pneumo-Pericardium  (J.  R.  Riddell)     -  -  -  424 

71ie  draivings  of  microscopic  stctions  are  by  Richard  Muir.     The  other  draivings 
are  hy  A.  K.  Maxwell. 


DISEASES  OF  THE  HEART 

CHAPTER  I 
THE  DISEASES  OF  THE  MYOCARDIUM 

The  Myocardium. — The  cardiac  muscle  is  very  specialized,  and 
differs  in  many  respects  from  voluntary  and  involuntary  muscle 
elsewhere.  The  cells  are  irregular  in  shape,  and  more  or  less 
rhomboidal  on  longitudinal  section,  and  divide  into  branches 
which  unite  directly  with  those  of  adjacent  cells.  There  is  no 
sarcolemma,  and  while  appropriate  staining  shows  the  junctions 
of  the  adjacent  cells  very  distinctly,  these  are  invisible  in  un- 
stained sections,  and  many  observers  are  inchned  to  regard  the 
cardiac  muscle  as  forming  a  syncytium.*  The  nucleus  is  large 
and  oval  in  shape,  with  a  well-marked  chromatin  network,  and 
lies  in  the  centre  of  the  cell  bounded  laterally  by  the  fibril 
bundles.  At  each  pole  Hes  an  ovoid  mass  of  undifferentiated 
protoplasm,  in  which  some  yellowish-brown  granules  are  usually 
situated.  The  fibril  bundles  run  longitudinally  and  show  a 
transverse  striation,  which  is  well  marked  in  contracted  muscle, 
though  in  extended  fibres  the  longitudinal  arrangement  is  more 
distinct. 

The  arrangement  of  the  muscular  layers  is  extremely  com- 
phcated.  In  the  auricles  two  main  layers  are  apparent — a 
superficial  circular  set  of  fibres  passing  from  one  auricle  to 
the  other,  and  a  deeper  longitudinal  layer  which  is  chiefly 
confined  to  one  chamber.  But  both  are  connected  with  the 
septum,  and  their  regular  arrangement  is  disturbed  where  the 
great  veins  join  on  the  posterior  walls. 

*  The  structure  of  the  congenital  tumours  of  the  heart  (rhabdomyomata) 
supports  this  theory,  for  each  cell  mass  contains  several  nuclei. 

1 


2  DISEASES  OF  THE  HEART 

The  arrangement  in  the  ventricles  is  more  complex.  The 
walls  are  much  thicker  than  those  of  the  am-icles,  but  the  thick- 
ness varies,  being  minimal  at  the  extreme  apex,  where  it  ma}^ 
only  measure  2  to  3  mm.;  and  maximal  in  the  upper  third 
of  the  left  ventricle,  where  it  may  measure  1  cm.  The 
septum  is  nearly  as  thick,  but  the  wall  of  the  right  ventricle  does 
not  exceed  5  mm.,  and  is  often  thinner.  The  muscular 
layers  next  the  endocardium  and  the  pericardium  are  in  a 
general  way  arranged  longitudinally.  The  superficial  layers 
run  obhquely  towards  the  apex,  and  then  turn  suddenly 
upwards  and  inwards  in  a  vortex,  and  ascend  on  the  inner 
surface.  The  central  bundles  are,  as  a  whole,  arranged  trans- 
versely :  some  interlace  in  the  septum  and  form  a  figure-of-eight 
loop  embracing  both  ventricles,  while  others  run  more  or  less 
obhquely  from  one  ventricle  to  the  other,  their  musculature 
being  thus  intimatety  commingled.  In  any  section  of  the 
ventricular  wall  a  few  fibres  are  found  to  be  cut  longitudinally 
and  a  few  transversely,  but  the  vast  majority  are  divided  more 
or  less  obliquely.  The  connection  of  the  muscle  of  the  two 
ventricles  is  thus  very  close,  and  contraction  of  one  side  is 
necessarily  accompanied  by  contraction  of  the  other.  It  is 
extremely  difficult,  how^ever,  to  appreciate  the  relations  of  the 
muscular  bundles  to  the  bloodvessels,  and  this  can  only  be 
followed  accurately  in  the  musculi  papillares,  whose  cells  are 
all  arranged  longitudinally. 

The  connective  tissue  in  the  normal  heart  is  extremely  scanty. 
There  are  thin,  loose  layers  beneath  the  endocardium  and  the 
pericardium,  and  the  two  are  connected  by  a  fine  meshwork^ 
which  surrounds  the  muscle  cells  and  supports  the  vessels  and 
nerves.  But  even  the  main  septa  are  small,  and  in  sections  the 
muscle  cells  seem  everywhere  in  close  apposition  to  each  other. 
The  connective  tissue  is,  however,  more  abundant  at  the  tips 
of  the  musculi  papiUares  where  they  join  the  chordae  tendinese, 
at  the  auriculo-ventricular  junction,  and  in  the  auricular 
appendices . 

The  Coronary  Circulation. — The  heart  is  supphed  with  blood 
by  the  coronary  arteries,  and  as  any  interference  with  their 
lumen  is  hkely  to  be  accompanied  by  serious  damage  to  the 
muscle,  their  anatomy  requires  consideration  in  some  detail. 


THE   DISEASES  OF  THE  MYOCARDIUM 


3 


The  right  coronary  artery  is  usually  the  smaller  of  the  two, 
and  arises  from  the  anterior  sinus  of  Valsalva.  It  passes  to 
the  right  in  the  auriculo-ventricular  groove,  giving  off  branches 
to  the  adjacent  muscle,  and  terminates  in  a  large  branch 
which  runs  downwards  in  the  posterior  interventricular  sulcus. 
It  supplies  blood  to  the  right  auricle  and  almost  the  whole 
of  the  right  ventricle,  and  to  the  posterior  parts  of  the  left 
ventricle  and  the  interventricular  septum. 

The  left  coronary  artery  arises  from  the  left  posterior  sinus 
of  Valsalva,  and  passes  to 
the  left  in  the  auriculo- 
ventricular  groove  ;  it  divides 
almost  at  once  into  two  main 
branches,  the  larger  of  which 
descends  in  the  anterior  in- 
terventricular sulcus,  while 
the  smaller  continues  its 
course  in  the  auriculo-ven- 
tricular groove.  These  sup- 
ply the  left  auricle,  the 
anterior  two-thirds  of  the 
interventricular  septum,  the 
bulk  of  the  left  ventricle, 
and  a  small  portion  of  the 
anterior  surface  of  the  right 
ventricle. 

The  main  horizontal  and 
vertical  branches  of  the  two 
arteries    anastomose     with 

each  other  at  their  extremities,  and  thus  form  around  the  heart 
two  rings  of  vessels  which  are  almost  at  right  angles  to  each 
other.  From  these  rings  smaller  arteries  penetrate  the  muscle, 
giving  off  still  smaller  vessels,  which  end  in  a  very  free  capillary 
system,  so  extensive,  indeed,  as  to  surround  each  individual 
muscle  cell  on  almost  every  side. 

The  coronary  arteries  send  a  few  smaU  branches  to  the  aorta 
and  the  pulmonary  artery;  and  an  anastomosis  with  corre- 
sponding branches  of  the  bronchial  arteries  has  been  described. 

Supplementary  coronary  arteries  are  frequently  met  with. 


Fig.  1. — Diagram  showing  the  Arterial 
Circulation  of  the  Normal  Heart. 


4  DISEASES  OF  THE  HEART 

sometimes  arising  witli  a  main  vessel  from  the  bottom  of  a 
small  pit  in  the  aortic  wall,  in  which  case  they  should  be  con- 
sidered to  be  merely  branches  with  an  abnormally  high  origin ; 
or  having  a  distinct  orifice  separate  from  that  of  the  main 
artery.  More  than  one  may  be  present,  and  occasionally  an 
artery  arises  from  each  of  the  three  sinuses.  The  importance 
of  supplementary  arteries,  however,  is  small,  as  they  are  at 
once  distributed  to  a  part  of  the  muscular  wall,  and  only 
represent  nutritive  branches. 

Variations  in  the  origin  of  the  coronary  arteries  are  not 
very  uncommon.  Both  coronary  arteries  sometimes  arise 
from  the  same  sinus,  either  as  one  trunk,  which  soon  divides, 
or  as  separate  vessels.  A  specimen  in  the  Western  Infirmary 
Museum  shows  this  latter  anomaly,  but  only  two  aortic  cusps 
are  present,  the  right  posterior  cusp  being  in  its  usual  situa- 
tion, while  the  left  posterior  and  the  anterior  are  fused  to- 
gether. Both  coronary  arteries  arise  in  the  latter  sinus,  the 
orifices  being  about  1'5  cm.  apart. 

A  few  cases  have  been  recorded  in  which  one  coronary 
artery  arose  from  the  aorta  and  one  from  the  pulmonary 
artery.  Brooks  has  reported  two  cases.  In  one  the  branches 
from  the  latter  vessel  were  distributed  to  the  pulmonary 
artery  and  to  the  right  ventricle;  in  the  other  no  branches 
were  supplied  to  the  heart,  the  vessel  at  once  entering  a 
cirsoid  mass  of  dilated  vessels  around  the  pulmonary  artery, 
where  it  was  joined  by  branches  from  the  right  coronary  artery, 
the  left  subclavian,  and  the  transverse  arch  of  the  aorta.  In 
both  cases  the  abnormal  vessel  arose  from  the  right  anterior 
sinus.  Krause  has  described  a  case  similar  to  Brooks's  first, 
save  that  the  artery  arose  from  the  left  anterior  sinus.  Abbott 
has  described  a  fourth  case  in  which  the  right  coronary  artery 
arose  in  its  normal  site,  and  directly  after  its  origin  expanded 
into  a  huge,  thick-walled  loop,  from  which  its  descending  and 
transverse  branches  arose.  The  left  aortic  coronary  artery 
was  absent,  but  a  large  thin-walled  trunk  emerged  from  the 
dilated  posterior  sinus  of  the  pulmonary  artery.  From  this 
vessel  branches  ran  downwards  along  the  front  of  the  inter- 
ventricular septum,  and  to  the  left  in  the  auriculo-ventricular 
groove.     A  fifth  specimen  is  present  in  the  museum  of    the 


THE  DISEASES  OF  THE  MYOCARDIUM  5 

Western  Infirmary.  The  right  coronary  artery  is  normal  in 
its  origin  and  distribution,  but  the  left  aortic  coronary  is 
absent,  while  an  artery  of  considerable  size  arises  from  the 
left  anterior  sinus  of  the  pulmonary  artery,  and  is  distributed 
mainly  to  the  left  ventricle.  In  none  of  these  cases  was  there 
any  other  congenital  cardiac  defect. 

Two  cases  have,  however,  been  recorded  where  the  aorta 
and  pulmonary  artery  were  transposed,  and  both  coronary 
arteries  arose  from  the  vessel  connected  with  the  right  ven- 
tricle, their  abnormal  origin  being  evidently  due  to  an  erroneous 
twist  in  the  development  of  the  septum  of  the  primitive  aorta . 
In  both  cases  death  ensued  within  a  short  period  after  birth. 
Three  of  the  first  group,  however,  lived  to  adult  age,  two, 
indeed,  being  elderly;  and  it  is  difiicult  to  understand  how 
the  nutrition  of  the  heart  was  maintained.  Brooks  has 
suggested  that  the  pulmonary  vessel  might  be  afferent  in 
nature,  and  Abbott  considers  that  this  might  apply  also  to  her 
case,  the  arterial  supply  being  confined  to  the  aortic  vessel. 

The  majority  of  cases  with  gross  disease  of  the  coronary 
arteries  show  more  or  less  change  in  the  cardiac  muscle,  for 
the  nutrient  arteries  are  end-arteries  in  Cohnheim's  sense,  and 
their  complete  obstruction  entails  the  death  of  the  area  which 
they  supply.  The  importance  of  the  anastomosis  between 
the  main  branches  has  not,  however,  been  fully  recognized. 
Sudden  and  complete  closure,  whether  experimental  or  patho- 
logical, produces  as  a  rule  an  infarct,  though  the  lesion  is 
smaller  than  the  area  anatomically  supplied  by  the  obstructed 
vessel  (Hirsch  and  Spalteholz);  but  if  the  closure  is  gradual, 
compensatory  dilatation  of  the  other  vessel  may  occur  and 
prevent  the  occurrence  of  any  lesion.  Several  cases  of  this  kind 
have  been  reported,  and  I  have  personally  examined  five 
specimens.  In  one  (Fig.  2)  the  descending  branch  of  the  left 
coronary  was  completely  obliterated  about  halfway  down  the 
interventricular  septum.  The  descending  branch  of  the  right 
coronary  artery  was  large  and  could  be  traced  round  the  apex, 
extending  upwards  in  the  anterior  interventricular  sulcus  for 
an  inch  or  more.  In  another  case  (Fig.  3)  the  orifice  of  the 
right  coronary  artery  was  invisible,  being  completely  blocked 


6 


DISEASES  OF  THE  HEART 


by  a  patch  of  aortic  atheroma.  The  artery  itself  was  greatly 
atrophied.  The  left  coronary  vessel,  on  the  other  hand,  was 
greatly  enlarged,  and  the  posterior  interventricular  artery 
arose  from  the  transverse  branch.  There  was  no  gross  lesion 
of  the  muscle,  though  microscopic  examination  showed  a  few 
small  patches  of  fibrosis,  and  as  the  patient  was  able  to  perform 
his  duties  until  ten  days  before  his  death,  the  anastomosis 
must  have  been  fairly  sufficient.     Huchard  and  Huchard  and 

Chiari  have  recorded  similar 
cases ;  and  Pagenstecher  has 
ligatured  the  right  coronary 
artery  during  an  operation 
without  evil  result. 

There  are  two  other  ways 
in  which  the  cardiac  muscle 
may  be  supplied  with  blood. 
The  foramina  Thebesii  are 
present   in  all  the  cavities 
of   the  heart,  though  they 
are  most  numerous  on  the 
right  side.     And  while  they 
are  generally  considered  to 
be  venous  in  character  and 
to    convey     blood    to    the 
auricles  and  ventricles,  the 
evidence  is  somewhat  incon- 
TiG.  2.— Diagram  SHOWING  THE  CoMPENSA-     pi,,„,Vp    „.-,.]    ^-v,p,,   mav  r^pr- 
TORY  Developments  of  the  Coronary     cmsive,  anci  tne}'    may  per 
Circulation    in   a   Case    where   the    haps  be  arterial  in  function. 
Descending    Branch    of     the    Left     p     xj.5  ,  •  j.  , 

Coronary  Artery  was  occluded.  Jrratt  S    experiments  are  m 

favour  of  the  latter  view, 
for  he  has  shown  that  the  hearts  of  dogs  may  continue  to 
contract  for  several  hours  after  removal  from  the  body,  even 
though  the  coronary  arteries  are  ligatured,  if  a  suitable  fluid  is 
allowed  to  pass  into  the  cardiac  cavities. 

There  is  also  evidence  that  the  endocardial  blood  may 
furnish  nourishment  to  the  adjacent  muscle,  for,  as  Muir  has 
pointed  out,  in  cases  of  healed  infarct  and  in  dystrophic 
fibrosis  a  thin  layer  of  muscle  always  persists  along  the  endo- 
cardial surface. 


THE  DISEASES  OF  THE  MYOCARDIUM 


It  is  weU  known  that  the  coronary  arteries  are  pecuKarly 
liable  to  pathological  processes ;  in  fact,  some  change  is  almost 
constantly  piesent  after  middle  life.  The  orifice  may  be 
obstructed  by  disease  of  the  aorta,  or  the  main  trunks  may 
show  patchy  atheroma  or  diffuse  fibrosis.  Such  changes  are 
readily  seen  on  naked- eye  examination,  but  the  condition  of 
the  larger  arteries  is  no  criterion  of  that  of  the  smaller,  whose 
walls  may  be  seriously  damaged  without  the  larger  vessels 
being  affected.  Most  com- 
monly both  sets  are  in- 
volved, but  the  degree  of 
the  lesions  is  by  no  means 
always  comparable. 

The  muscle  at  the  apes, 
that  next  the  endocardium, 
and  the  musculi  papillares 
in  particular  are  supplied 
by  the  longest  branches  of 
the  coronary  arteries,  and 
will  show  most  often  and 
in  greatest  degree  any 
lesions  Avhich  are  due  to 
interference  with  the  blood- 
supply.  Under  normal  con- 
ditions the  work  performed 
by  the  left  ventricle  is  much 
greater  than  that  done  by 
the  right,  but  in  many 
diseases  (emphysema,  mitral 
stenosis,     etc.)     the    right 

ventricle  is  overworked,  and  it  is  often,  in  consequence,  hyper- 
trophied.  Given  a  deterioration  of  the  blood,  whether  in  quantity 
or  quahty,  the  effect  upon  the  muscle  will  be  more  manifest,  and 
wiU  appear  first  where  the  blood-supply  is  least  ample,  and 
where  the  greatest  functional  activity  obtains.  And  these,  it 
will  be  seen,  are  the  cardinal  factors  in  determining  the  site  of 
almost  all  the  focal  lesions  which  occur  in  the  myocardium. 

Hypertrophy — Atrophy. — The    muscle   cells    in   the   normal 
heart  vary  considerably  in  size,  those  on  the  left  side  being 


Fig.  3. — Diagram  showing  the  Compensa- 
TOKY  Developments  of  the  Coronaey 
Circulation  in  a  Case  where  the 
Right  Coronary  Artery  was  occluded 
AT  ITS  Origin. 


8 


DISEASES  OF  THE  HEART 


appreciabl}^  larger  than  those  on  the  right,  and  the  cells  jn  the 
auricles  are  smaller  than  those  in  the  ventricles.  There  is 
often  considerable  difference  even  between  adjacent  cells,  and 
it  may  be  difficult  to  estimate  the  average  size  in  anj'  particular 
case.  It  is,  however,  always  greater  than  normal  in  hyper- 
trophied  hearts,  the  increase  being  chiefly  in  the  transverse 
diameter,  and  in  other  respects  the  cells  seem  normal.  There 
has  been  considerable  discussion  as  to  whether  the  celLs  are 
more  numerous  as  well  as  larger,  and  the  question  is  still  un- 
settled. Most  observers  (Gotch,  Hirschfelder)  are  against 
any  numerical  increase,  but  G.  A.  Gibson  accepted  Zielonko's 
work  as  conclusive  evidence  on  the  other  side.     The  connective 

tissue,  too,  in  hypertrophied  hearts 
is  always  increased  in  amount. 

In  atrophied  hearts  the  cells'may 
be  considerably  smaller  than  usual. 
In  some  cases  no  other  abnor- 
mahty  can  be  detected,  but  in 
others  the  perinuclear  pigment  is 
excessive.  In  the  normal  heart 
pigment  granules  appear  about 
the  age  of  ten,  and  their  number 
increases  with  advancing  years  ; 
the}^  are  usually  numerous  in 
senile  muscle.  They  are  said  to 
be  composed  of  hsematoidin,  and 
are  brownish-yeUow  in  colour  and 
of  varying  size.  They  lie  in  conical 
masses  at  each  pole  of  the  nucleus  in  the  perinuclear  space. 
Their  significance  is  obscure.  In  atrophy  they  may  be  numerous 
or  very  scanty, 

Ischaemic  Atrophy. — In  extreme  cases  of  simple  atrophy 
and  in  cases  of  local  starvation  from  obstruction  of  the  coronary 
arteries,  other  changes  may  be  noticed  in  the  cells.  In  the 
latter  case  the  size  of  the  cells  varies,  those  around  the  arterioles 
being  httle  smaller  than  normal,  while  those  a  little  distance 
away  are  distinctly  diminutive.  They  are,  too,  empty  in 
appearance,  the  central  fibril  bundles  having  disappeared, 
leaving  only  a  few  at  the  periphery  of  the  cell  (Fig.  4).     The 


-IscHJEMic  Atrophy. 
( X  120.) 

The  cells  nearest  to  the  thickened 
endocardium  are  least  altered. 


Fig.  4. 


THE  DISEASES  OF  THE  MYOCARDIUM  9 

perinuclear  mass  is  large  and  stains  faintly,  and  the  lesion 
is  readily  appreciated  in  both  longitudinal  and  transverse 
sections.  The  nucleus  is  always  abnormal,  and  is  at  first  large 
vdth.  a  scanty  chromatin  network,  which  may  be  here  and  there 
aggregated  into  httle  clumps ;  while  in  the  later  stages,  when 
the  ceU  is  disappearing,  it  becomes  minute  and  pyknotic. 

Granular  Degeneration. — Granular  degeneration  (cloudy 
swelling)  is  in  some  ways  comparable  to  ischsemic  atrophy. 
In  the  early  stages  the  proper  detail  of  the  ceU  is  obscured  by 
somewhat  coarse  granules,  which  are  scattered  widespread 
over  the  cell,  though  they  are  most  numerous  in  the  central 
parts  where  the  striation  is  almost  lost.  But  in  the  later 
stages  (Fig.  5)  the  cells  become  smaller  and  the  perinuclear 
mass  enlarged,  only  a  few  fibrils  with  poorly  marked  striation 
persisting  at  the  periphery ;  while  still  later  all  trace  of  stria- 
tion has  disappeared,  and  a  granular  mass  of  an  irregular  oval 
shape  alone  remains.     In  ischajmic  atrophy  the  fibril  bundles 


'mUTiWTM—    ~"'V~i'T~ili''iiii  Mi"riMiiiii''iir' 


Fig.  5. — Granular  Degeneration  in  an  Advanced  Stage,     (x  1,000.) 

always  show  transverse  striation  so  long  as  they  are  recog- 
nizable as  definite  muscle  cells.  In  granular  degeneration  the 
striation  is  obscured  at  a  very  early  period,  even  before  the 
cells  begin  to  atrophy. 

Granular  degeneration  occurs  in  the  acute  infections,  and  is 
most  extreme  in  cases  where  the  illness  has  lasted  for  more 
than  a  few  days.  It  is  often  accompanied  by  some  degree  of 
fatty  and  hyahne  degeneration. 

Hyaline  Degeneration. — H3'aline  degeneration  is  compara- 
tively uncommon.  The  affected  ceUs  are  homogeneous  and 
glistening  in  appearance,  and  displaj^  none  of  the  characteristic 
features  of  the  cardiac  muscle,  the  nucleus  and  the  striation 
having  disappeared.  The  staining  reactions  are  altered,  and 
the  cells  colour  yellow  instead  of  red-brown  vrith.  Ehrhch's 
triple  stain.  The  distribution  of  the  change  varies.  Some- 
times only  a  part  of  a  cell  is  affected ;  more  often  a  whole  ceU 


10  DISEASES  OF  THE  HEART 

or  a  group  of  contiguous  cells.     And  while  as  a  rule  the  area 
involved  is  small,  it  is  sometimes  large  and  widespread. 

Hyaline  degeneration  is  evidently  a  coagulation  necrosis, 
and  is  always  present  in  recent  infarcts  of  the  heart ;  but  it 
may  also  be  produced  by  toxic  causes,  as  it  can  always  be 
seen  in  the  immediate  vicinity  of  inflammatory  foci,  and  may 
be  found  in  a  few  cells  in  the  acute  infections. 

Dissociation. — The  cells  of  the  heart,  when  examined 
microscopically,  are  often  seen  to  be  dissociated.  Sometimes 
the  cleavage  takes  place  along  their  line  of  junction  (segmenta- 
tion), each  cell  lying  separate  from  its  neighbom*s ;  and  some- 
times it  occurs  through  the  cells  themselves  (fragmentation). 
The  change  may  be  discrete  and  limited,  or  ma}'^  be  widespread. 

It  has  been  suggested  that  dissociation  (fragmentation  in 
particular)  is  merely  an  artefact  occurring  during  section 
cutting ;  at  any  rate,  appearances  evidently  due  to  this  cause 
are  often  met  with  locally;  but  when  it  is  widespread,  it  is 
probably  vital  in  origin.  It  is,  however,  present  in  some 
degree  in  the  majority  of  hearts  which  are  examined,  and  it 
has  been  found  in  atrophied  and  in  hypertrophied  hearts,  in 
hearts  which  are  degenerate  and  in  hearts  which  are  sound, 
and  in  particular  in  the  hearts  of  individuals  whose  death  has 
been  sudden  and  abrupt  (trauma,  hanging,  etc.).  Its  presence 
seems,  then,  to  be  of  little  importance,  and  it  is  probably  due, 
as  V.  Recklinghausen  suggested,  to  irregular  and  perhaps 
excessive  contraction  of  the  cardiac  muscle  during  the  death 
agony.  It  is  in  no  way  the  cause  of  death,  but  rather  its 
result. 

Fatty  Infiltration. — There  is  always  some  fat  in  the  sub- 
pericardial  connective  tissue,  the  amount  var3ang  in  different 
cases,  being  sometimes  very  scanty  and  sometimes  so  con- 
siderable that  it  covers  and  obscures  the  ventricular  muscle. 
It  is  normally  thickest  in  the  auriculo-ventricular  sulcus,  and 
over  the  right  heart. 

Under  pathological  conditions  the  fat  is  sometimes  found 
to  be  infiltrating  the  muscle,  spreading  along  the  main  fibrous 
septa,  in  particular  around  the  bloodvessels,  and  even  between 
individual  muscle  fibres.     As  a  rule  the  infiltration  is  con- 


THE  DISEASES  OF  THE  MYOCARDIUM  11 

fined  to  tlie  superficial  layers,  but  in  some  cases  it  may  pene- 
trate the  muscular  Avail,  and  in  advanced  stages  the  fat  may 
■even  be  visible  in  httle  patches  beneath  the  endocardium. 
Whenever  the  external  fat  is  excessive,  some  infiltration  always 
obtains,  but  marked  infiltration  may  occur  without  notable 
•excess  of  the  superficial  fat.  Fatty  infiltration  is  always 
most  extreme  on  the  right  side  of  the  heart,  where  it  is  often 
considerable  when  the  left  side  is  but  little  affected. 

In  normal  hearts  one  or  two  laj-ers  of  muscle  cells  in  the 
immediate  vicinity  of  the  superficial  fat  always  show  some 
fatty  degeneration,  but  the  change  is  strictly  limited.  In  fatty 
infiltration  a  similar  condition  obtains,  but  to  a  far  greater 
-extent,  and  a  majority  of  the  muscle  cells  may  be  involved. 

Fatty  infiltration  is  usually  a  part  of  a  general  tendency 
to  obesity.  In  exceptional  cases  whose  nature  is  not  under- 
stood, it  may,  however,  affect  the  heart  alone. 

Fatty  Degeneration. — Fatty  infiltration  is  readily  appre- 
•ciatecl  on  naked-eye  examination,  but  fatty  degeneration 
frequently  can  only  be  recognized  microscopically,  even  in 
•cases  where  it  is  well  marked ;  for  the  colour  changes  by  which 
its  presence  is  known  may  be  obscured  in  hearts  whose  blood- 
vessels are  congested,  in  hypertrophied  and  atrophied  hearts, 
and  in  jaundice.  Special  staining  methods,  too,  are  required, 
for  by  the  usual  methods  of  preparation  the  fat  is  dissolved 
out  of  the  cells,  and  although  the  honeycomb  appearance  in 
extreme  cases  is  quite  distinctive,  the  lesser  degrees  are  readily 
missed.  Fatty  degeneration  is  extremely  common,  but  the 
frequency  of  its  occurrence  is  considerably  underestimated 
on  account  of  the  want  of  the  special  technique  necessary  for 
its  detection. 

In  a  typical  case  the  appearance  of  the  heart  is  very  character- 
istic, many  minute  spots  of  buff  or  yellow  colour  being  scattered 
over  the  endocardial  surface  in  an  irregular  wa}^  The 
motthng  is  sometimes  very  fine  and  more  or  less  diffuse,  but 
more  commonly  the  spots  are  massed  together,  forming  bands 
which,  on  the  papillary  muscles,  run  transversely.  These 
bands  are  irregular  and  often  zigzag  in  contour,  and  when 
distinct,  are  aptly  compared  to  the  markings  on  a  thrush's 
breast.     The  colour  change  is  usually  apparent  onty  beneath 


12  DISEASES  OF  THE  HEART 

the  endocardium,  and  on  section  is  seen  to  penetrate  for  but 
a  short  distance  into  the  muscle,  and  to  fade  gradualh^  away. 
But  occasionally  it  involves  the  whole  wall,  and  may  even  be 
seen  beneath  the  pericardium.  Very  rarel}-  it  is  apparent  only 
on  the  pericardial  surface. 

The  whole  of  the  heart  is  never  equally  affected,  and  most 
frequently  only  a  part  is  involved.  It  is  most  common  in  the 
left  ventricle,  less  so  in  the  right,  and  it  occurs  but  rarely  in 


Fig.  6. — Fatty  Degenekation  :    Paka-Arterial  Distribution,     (x  200.) 
(From  a  case  of  ansemia.) 

the  auricles.  One  ventricle  may  be  extensively  diseased,  and 
the  other  but  slightl}-.  In  the  left  ventricle  the  papillary 
muscles,  the  adjacent  muscle  on  the  posterior  waU,  and  the- 
septum  are  most  often  degenerate ;  on  the  right  side  the  papillary 
muscles  and  the  muscle  in  their  vicinity.  The  left  ventricle 
suffers  alone,  or  to  the  greatest  extent,  in  anaemia  and  aortic 
valvular  disease.  In  chronic  pulmonarj^  disease  and  in  mitral 
affections  the  right  ventricle  is  chiefly  involved. 

On  microscopic  examination  of  sections  stained  with  osmie 


THE  DISEASES  OF  THE  MYOCARDIIBI  13 

acid,  the  fatty  granules  are  seen  to  be  distributed  irregularly 
within  the  ceUs,  being  largest  and  most  numerous  in  the 
central  parts  around  the  nucleus ;  but  even  in  advanced  cases 
the  whole  of  the  muscle  fibrils  are  never  destroyed.  Eatty 
degeneration  does  not  affect  the  size  of  the  cell,  and  may  be 
present  in  cells  which  are  larger  or  smaller  than  normal. 

Examination  Avith  a  low  power  distinguishes  two  forms. 
In  one  (thrush  breast)  the  distribution  of  the  fatty  ceUs  is  very 
irregular,  little  islets  of  more  or  less  normal  cells  being  sur- 


FiG.  7. — Fatty  Degexeeatiox  :    Diffuse  Foem,  of  Toxic  ORiors'.     (x  200.) 

rounded  on  all  sides  by  masses  of  degenerate  cells  (Eig.  6). 
As  a  rule  the  transition  is  gradual,  but  sometimes  a  cell  whoUy 
free  from  fat  may  he  next  one  which  is  extensively  disorganized. 
Sometimes  almost  every  cell  is  fatty,  but  a  patchy  distribution 
is  stiU  apparent,  islets  of  ceUs  with  comparatively  little  change 
lying  "^-ithin  areas  whose  ceUs  are  greatly  altered.  In  sections 
of  the  walls  it  is  often  difficult  to  determine  the  relationship 
of  the  islets  to  the  bloodvessels,  but  in  sections  of  the  muscuh 
papillares,  where  the  ceUs  are  arranged  longitudinally,  it  can 
be  seen  that  those  around  the  arterioles  are  less  affected  than 


14  DISEASES  OF  THE  HEART 

those  farther  awaj'  (para-arterial  distribution).  In  the  second 
form  the  fatty  change  is  generally  less  extreme  than  it  is  in 
the  former,  but  it  is  diffuse  and  almost  equally  distributed 
(Fig.  7). 

The  patchy  degeneration  is  seen  in  its  most  exquisite  form 
in  the  left  ventricle  in  cases  of  anaemia,  and  it  is  always  best 
marked  on  the  musculi  papiUares.  It  occurs,  therefore,  in 
those  muscle  cells  which  are  most  distant  from  their  nutrient 
arterioles,  and  in  the  parts  of  the  ventricle  supplied  by  the 
longest  branches  of  the  coronary  arteries ;  and  it  is  evidently 
due  to  a  relatively  insufficient  supply  of  blood,  arising  partly 
from  the  blood  condition,  and  partly  from  the  anatomical 
distribution  of  the  vessels.  In  cases  where  the  maximal  change 
is  situated  elsewhere,  a  special  reason  for  the  particular  site 
can  usually  be  found.  Thus,  in  a  case  of  aortic  valvular 
disease,  the  right  ventricle  was  found  to  be  more  fatty  than 
the  left,  but  the  orifice  of  the  right  coronary  artery  was  partly 
occluded  by  aortic  atheroma.  In  another  case,  that  of  a  child 
who  died  somewhat  suddenly  a  few  days  after  a  burn,  the 
right  ventricle  was  again  more  fatty  than  the  left ;  but  as  the 
patient  was  at  the  time  of  the  burn  suffering  from  bronchitis, 
the  right  ventricle  was  overtaxed,  and  the  lesion  was,  in  conse- 
quence, situated  at  the  point  of  greatest  functional  strain. 

The  diffuse  degeneration  is  of  toxic  origin.  In  local 
toxaemias,  such  as  occur  in  abscess  and  pericarditis,  a  few  fatty 
cells  can  always  be  seen  in  the  vicinity  of  the  lesion,  and  a 
diffuse  degeneration  can  be  readily  produced  in  animals  by 
the  administration  of  chloroform  and  phosphorus.  In  such 
experiments  the  animals  may  die  rapidly,  in  which  case  the 
degeneration  is  slight  and  periarterial  in  distribution,  or  may 
survive  for  several  days,  when  it  is  invariably  widespread  and 
uniform. 

CUnically  it  is  particularly  associated  with  severe  anaemia, 
emphj^sema,  chronic  renal  disease,  and  alcoholism.  In  the 
ordinary  work  of  a  laboratory  it  is  difficult  to  secure  "pure  " 
cases  of  chronic  alcoholism,  as  many  causes  may  have  co- 
operated in  producing  death;  but  in  one  case  which  I  have 
examined  the  association  seemed  definite.  A  man,  who  had 
been  drinking  heavily  for  a  fortnight,  was  crushed  between 


THE  DISEASES  OF  THE  MYOCARDIUM  15 

a  cart  and  a  wall,  and  died  within  a  few  hours  from  rupture 
of  a  kidney  and  fractured  ribs.  His  heart,  which  seemed 
normal  on  macroscopic  examination,  proved  to  be  the  seat 
of  an  extensive  and  diffuse  fatty  degeneration. 

A  diffuse  degeneration  is  not  absolutelj^  uniform  in  its 
distribution,  and  some  parts  of  the  heart  always  show  more 
change  than  others;  but  this  is  not  fatal  to  the  general  con- 
tention. The  very  special  arrangements  of  the  muscular 
fibres  and  of  their  vascular  supply  are  adapted  to  secure  the 
successful  performance  of  work  which  varies  greatty  in  its 
amount  from  time  to  time,  and  which  may  be  at  a  maximum 
in  either  ventricle  under  certain  circumstances.  It  seems 
probable,  too,  that  in  normal  conditions  the  whole  of  each 
ventricle  is  not  called  upon  to  perform  an  equal  amount  of 
work,  and  given  a  blood  poison,  it  wiU  act  most  rapidly  on 
those  parts  which  are  working  nearest  to  their  maximum 
capacity ;  for  ceUs  working  well  within  their  power  will  require 
less  nourishment,  and  will  suffer  to  a  less  degree  from  any 
vitiation  of  the  blood.  The  causes  of  death  are  often  multiple, 
pneumonia,  for  example,  showing  a  maximal  mortality  in 
alcohohcs  and  persons  with  degenerate  tissues ;  and  an  acute 
infection  is  often  the  terminal  event  in  a  case  of  chronic  renal 
disease  where  the  coronary  arteries  are  not  as  supple  as  normal, 
and  perhaps  have  a  narrow  lumen.  In  such  a  case  it  is 
difficult  to  predict  the  precise  locality  of  maximal  strain  or 
to  estimate  the  relative  value  of  the  different  factors — anaemia, 
toxaemia,  high  blood-pressure — which  maj^  be  active  in  pro- 
ducing the  condition. 

The  Fibroses  of  the  Heart. — The  connective  tissue  of  the 
heart  is  not  infrequently  increased  in  amount,  but  the  fibrosis 
is  never  uniform  in  distribution,  being  scattered  in  httle  islets 
or  bands  irregularly  throughout  the  muscle.  Sometimes  only 
a  single  patch  is  present,  but  more  frequently  there  are  several, 
and  they  may  be  very  numerous.  They  may  be  of  any  size 
or  shape;  sometimes  mere  pin-points,  and  sometimes  blocks 
an  inch  or  more  thick ;  often  rounded,  or  oval,  or  star-shaped ; 
sometimes  a  long  ribbon;  their  greatest  diameter  usually 
corresponding  with  the  general  direction  of  the  muscle  fibres. 


16  DISEASES  OF  THE  HEART 

Their  consistence  varies  with  their  age,  recent  nodules  being 
soft  and  vascular,  and  the  cut  surface  being  flush  with  the 
surrounding  muscle;  while  the  older  patches  are  firm  and 
depressed,  and  the  surrounding  muscle  stands  out  prominently 
around  them.  If  a  large  area  of  the  wall  is  involved,  it  is 
often  notably  thinned,  and  may  only  measure  a  quarter  of  its 
normal  thickness  (Fig.  8). 

Fibroid  patches  are  most  commonly  found  in  the  left 
ventricle,  though  they  may  occur  anywhere.  They  are  rarely 
met  with  on  the  right  side.  The  musculi  papillares  are  most 
frequently  affected  and  are  often  shrunken  and  deformed ;  and 
then,  in  order,  the  apical  third  of  the  left  ventricle,  the  lower 
part  of  the  septum,  and  the  posterior  wall  of  the  left  ventricle 
about  the  junction  of  its  upper  and  middle  third.  The  most 
usual  sites  in  the  right  ventricle  are  the  musculi  papiUares  and 
the  apex.  The  patches  are  generally  situated  deeply  in 
the  muscle,  the  ribbon  form  often  lying  about  the  junction 
of  the  inner  and  middle  third  of  the  wall,  and  do  not  always 
extend  to  the  surface;  but  in  extreme  cases  the  overlying 
endocardium  is  thick  and  opaque,  and  the  visceral  pericardium 
may  be  similarly  involved  and  sometimes  adherent  to  its 
outer  layer.  In  lesser  degrees  one  or  other  covering  may  alone 
be  impHcated. 

Fibrosis  is  most  frequently  the  result  of  obstruction  of  the 
coronary  arteries.  These  vessels  supply  practically  the  whole 
of  the  cardiac  muscle,  and  the  nutrient  vessels  are  end-arteries, 
although  the  main  trunks  anastomose.  Obstruction  of  the 
former,  therefore,  necessarily  causes  necrosis  of  the  tissues 
which  they  supply,  though  obstruction  of  the  latter  may  be 
compensated  by  anastomotic  developments ;  but  as  the  anas- 
tomoses are  slight,  unless  the  occlusion  is  gradual  in  its  onset 
the  muscle  is  generally  more  or  less  damaged.  If  the  occlu- 
sion is  sudden,  the  lesions  are  always  considerable. 

Infarct — Myomalacia  Cordis. — The  nutrient  arteries  may  be 
occluded  by  emboli  or  thrombi,  the  latter  being  more  common. 
The  tissues  which  are  involved  necrose,  and  if  the  patient 
survives,  are  gradually  absorbed  and  replaced  by  connective 
tissue.  Large  infarcts  are  generally  due  to  sudden  occlusion 
to  a  main  artery,  the  abruptness  of    the  closure  preventing 


Fig.  8.     Fibrosis  of  the  Anterior  Wall  of  the  Left  Ventricle 
W.I.  Museum. 


THE  DISEASES  OF  THE  MYOCARDIIBI  17 

tlie  successful  development  of  the  anastomotic  connections. 
They  occur  towards  the  peripheral  distribution  of  the  main 
vessels,  near  the  apex  between  the  extremities  of  the  descend- 
ing branches,  and  on  the  posterior  wall  of  the  left  ventricle 
in  the  area  between  the  extremities  of  the  transverse  branches. 
The  whole  of  the  muscle  fibres  never  disappear  in  these  cases, 
a  few  cells  always  persisting  along  the  margins  of  the  walls 
(Fig.  9),  those  along  the  inner  aspect  being  kept  aUve  by  the 

-    ■;■  -     .      ;***>J'»>    ■■ 


^' 


Pericardium.  Endocardium. 

Fig.  9. — Dysteophic  Fibrosis  of  Wall  op  Left  Venteicle.     (x  20.) 
Some  muscle  cells  still  persist  along  tlie  pericardial  and  the  endocardial  margins. 

endocardial  blood,  and  those  on  the  outer  by  the  superficial 
subpericardial  anastomosis. 

The  appearance  of  infarcts  varies.  They  may  be  dull  yellow 
in  colour  from  fatty  changes  (Fig.  11),  or  uniformly  red  or 
mottled  from  extravasation  of  blood.  White  infarcts  are 
usually  fairly  firm  in  consistence,  but  some  are  soft  and  friable 
from  the  development  of  autolytic  processes.  Haemorrhagic 
infarcts  are  soft  and  may  be  almost  diffluent,  in  Avhich  case 
rupture  of  the  heart  is  not  unusual. 

Para-Arterial  (Dystrophic)  Fibrosis. — Partial  occlusion  of  the 
arteries,  or  complete  obstruction  of  gradual  onset,  leads  to 
somewhat  similar  results,   the  muscle  cells  suppHed  by  the 

2 


18  DISEASES  OF  THE  HEART 

particular  branch  which  is  affected  suffering  in  nutrition,  and 
in  extreme  cases  gradually  atrophying  and  being  replaced  by 
connective  tissue.  The  process  is  seen  best  in  well-marked 
examples  in  the  papillary  muscles,  as  their  cells  are  arranged 
longitudinally. 

^Microscopic  sections  (Fig.  10)  show  that  the  distribution  of 
the  fibrosis  is  exactty  similar  to  that  of  the  fat  in  the  para- 
arterial  form  of  fatty  degeneration,  little  islets  of  more  or 
less  normal  muscle  being  embedded  in  diffuse  patches  of  fibrous 
tissue.     In  the  centre  of  the  muscular  islet  around  the  arteriole 


)^;.-. 

"^^'^                '•"   9 

.^.  -,' 

.« 'jft 

■•#  ■ 

••       ■^*.-'  -.•' 


.- "r*','^*^  *■*■:- 


-»      ,  ■  ii  ■  .■ 

.*.■■•.'■•■'   '   '  ■        '    », 

s.  " 

-•  Si  ■ 


FiG.  10. — Paea-Aeterial  (Dystrophic)  Fibrosis.     (x50.  ) 

the  muscle  cells  may  be  normal,  but  those  at  the  periphery 
show  every  grade  of  ischaemic  atrophy,  and  are  widely 
separated  from  each  other.  In  the  centre  of  the  fibrotic  area 
the  connective  tissue  is  sparsely  nucleated  and  often  hyaline^ 
with  few  bloodvessels,  but  in  the  vicinit}^  of  "the  muscle  it 
may  be  thickly  nucleated  and  very  vascular.  Little  collections 
of  pigmentary  debris  may  be  visible. 

In   both  infarct  and  para-arterial  fibrosis   the  process   is 
clearly  dystrophic,  the  muscular  degeneration  being  primary 


Fig.  11.     Marked  Xarrowixg  of  the  Orifices  of  the  Coronary  Arteries 

FROM  Syphilitic  Disease  of  the  Aorta.    Infarct,  with  Fatty 

Degeneration  of  the  Walls  of  the  Left  Ventricle.    R.I.  Museum. 


THE  DISEASES  OF  THE  MYOCARDIUM 


19 


and  the  fibrous  overgrowth  its  result;  and  in  both  cases  the 
change  is  patchy  and  rarely  of  ribbon  shape.  The  ultimate 
result,  too,  is  similar,  and  in  old-standing  cases  the  precise 
mechanism  of  the  process  cannot  be  distinguished.  Their 
usual  cause  is  endarteritis,  but  they  may  follow  occlusion  of 
the  orifice  of  a  coronary  artery  by  a  patch  of  atheroma  in  the 
aorta,  as  in  the  case  reported  by  Gibson  and  Muir,  and  in  one 
which  I  have  personaU}-  observed.  But  coronary  disease 
does  not  necessarily  cause  fibrosis.  This  only  ensues  when 
the  lumen  of  the  vessel  is  narrowed  or  occluded,  and  the  main 
trunks  are  often  larger  than   normal  when  their  walls  are 


Fig.  12. — Periaeterial  Fibrosis,     (x  50.) 

diseased,  the  weakening  of  the  wall  inducing  dilatation; 
though  when  the  smaller  vessels  are  affected,  the  lumen  is 
generally  narrowed. 

Periarterial  Fibrosis. — In  some  cases  of  fibrosis  the  new- 
formed  connective  tissue  is  situated  immediately  around  the 
arteries  (Fig.  12),  and  this  periarterial  fibrosis  must  be  clearly 
differentiated  from  that  which  has  just  been  described,  for  it 
is  due  to  entirely  cliff' erent  causes. 

The  adventitia  of  the  normal  artery  is  sharph'  demarcated 
on  one  side  by  the  muscle  cells  of  the  media,  but  on  the  other 
cannot  be  accurately  defined,  as  it  blends  with  the  general 
connective  tissue  of  the  heart.     In  certain  cases  of  fibrosis 


20 


DISEASES  OF  THE  HEART 


the  connective  tissue  around  the  arteries  is  notably  excessive, 
and  forms  an  oval  or  a  star-shaped  mass  of  varying  size.  In 
the  smaller  patches  the  muscle  in  the  vicinity  may  not  be 
imphcated  in  the  process,  but  in  the  larger  patches  the  strands 
pass  in  between  the  muscle  cells  and  separate  them  from  each 
other  (Figs.  13,  14).  In  early  cases  (Fig.  13)  the  connective 
tissue  may  be  vascular  and  very  cellular,  but  in  older  examples 
(Fig.  14)  it  is  often  hyaline  and  sparsely  nucleated. 

Periarterial  fibrosis  is  generally  less  gross  and  more  diffuse 
than  the  para-arterial  type,  and  is  sometimes  of  ribbon 
iorm. 

Inflammatory  lesions  are  not  infrequently  present  in  the 
walls  of  the  heart.     It  is  unusual  to  fmd  large  abscesses,  for 


■^  . 


Fig.    IS.-r-^EW^-FOEMED    eONJfECTIVE   TiS&UE    IN    THE    ViCINITY 

OF  AN  Arteriole.     (x500.) 
(From  a  cas,^  of  malignant  endocarditis. ) 

patients  suffering  from  pyaemia  with  metastatic  deposits  in 
this  situation  generally  die  early,  but  microscopic  abscesses 
are  not  uncommon,  and  are  often  present  in  mahgnant  endo- 
carditis. They  are  frequently  due  to  direct  extension  of  the 
infection  from  the  base  of  the  affected  valve ;  and  are  occasion- 
ally found  a  little  distance  away  beneath  a  patch  of  mural 
endocarditis ;  and  they  may-  be  disseminated  fairly  widely  in 
the  substance  of  the  muscle  from  infection  of  the  coronary 
blood.  In  the  majority  of  cases  of  this  kind  death  ensues 
during  the  period  of  infection,  but  in  a  small  minority  recovery 
ensues,  and  the  scar  beneath  a  thickened  patch  on  the  endo- 


THE  DISEASES  OF  THE  MYOCARDIIDI  21 

cardiiim  reveals  the  nature  of  the  process.  It  is  conceivable 
that  some  examples  of  myocardial  fibrosis  may  result  from 
infective  lesions,  but  the  unfavourable  result  in  such  cases 
renders  it  improbable  that  this  cause  is  often  active. 

In  some  cases  of  chronic  mitral  disease  the  inflammatory 
lesion  is  not  strictly  limited  to  the  valves,  and  the  cusps,  the 
chordae  tenclinse,  and  the  papiUarj^  muscles  are  aU  welded 
firmly  together  into  a  more  or  less  hard  fibroid  mass  (the 
typical  funnel-shaped  mitral  stenosis,  Fig.  139).  The  fibrosis 
in  these  cases  is  rarely  confined  to  the  parts  already  men- 
tioned, but  also  extends  from  the  base  of  the  valves  into  the 


^  jS^^  ^^    '^zL  *z*     ^       is^^^ 


Fig.  14. — Perifascicixlaii  Fibeosis.     (x200.) 

adjoining  muscle  in  the  direction  of  theoentral  fibrous  body ;  and 
a  patchy  fibrosis  in  the  substance  of  the  muscle  often  coexists. 
It  has  been  known  for  long  that  the  rheumatic  infection  has 
a  special  predilection  for  the  cardiac  valves,  and  is,  indeed, 
the  most  common  cause  of  chronic  valvular  disease;  and  it 
is  also  recognized  to  be  a  frequent  cause  of  the  subcutaneous 
nodules  which  occur  in  childhood.  The  earher  writers  who 
first  noticed  this  association  failed  to  appreciate  its  full 
significance,  but  the  researches  of  Barlow  and  Warner  and 
Cheadle  showed  that  there  was  a  close  connection  between 


22  DISEASES  OF  THE  HEART 

the  occurrence  of  endocarditis  and  the  eruption  of  nodules, 
and  that  the  presence  of  large  subcutaneous  ncdules  was  an 
invariable  sign  of  serious  valvular  involvement.  In  1899 
Pojaiton  demonstrated  the  existence  in  the  cardiac  muscle 
in  cases  of  acute  rheumatism  of  minute  nodules,  which  were 
exactly  comparable  to  those  found  beneath  the  skin,  and 
subsequent  observers  have  emphasized  the  frequency  and  the 
multiphcity  of  these  lesions.  The  nodules  are  invariably 
small,  and  are  generally  invisible  on  naked-eye  examination. 


^^[i^^,  ;^;v:■:-i,•^^:N::^■;;,■ 


Fig.  15. — Round-Celled  Infiltration  of  the  Myocardium:  Focal  Form. 

(X  90.)     (A.  M.  K.) 

They  occur  most  frequently  in  the  ventricles,  especially  on 
the  left  side,  and  are  generally  situated  in  the  vicinity  of,  or 
around,  an  arteriole. 

jNIicroscopic  examination  shows  that  the  essential  lesion  is 
a  round-celled  infiltration  of  the  interstitial  tissue.  It  is 
situated  around  an  arteriole  or  in  its  immediate  vicinity,  and 
sometimes  involves  the  vessel  wall,  which  may  be  so  swollen 
that  the  lumen  is  narrowed.  The  cells  may  be  few  in  number 
and  the  adjacent  muscle  apparently  normal;  but  if  they  are 


THE  DISEASES  OF  THE  MYOCARDIUM 


23 


numerous,  tliey  inj&ltrate  between  the  muscle  cells,  whicli  in 
this  case  are  degenerate.  In  most  cases  the  cells  are  arranged 
in  discrete  foci,  perhaps  widely  separated  from  each  other 
(Fig.  15);  but  in  others  the  infiltration  is  diffuse  (Fig.  16), 
and  larger  areas  are  involved.  The  cells  are  mainl^^  mono- 
nuclear, the  majority  being  evidently  lymphocytes,  but  a  few 
larger  ceUs  with,  a  fair  amount  of  protoplasm,  which  are 
probabty  of  connective-tissue  origin,  are  often  present;  and 
occasionally  a  few  multinucleated  giant  cells.     A  few  poly- 


FiG.  16. — Rouxd-Celled  Infiltratiok  of  the  Myocardium:  Diffuse 
Form,     (x  90.)     (A.  M.  K.) 

morphonuclear  cells,  too,  may  be  found.  These  cellular  in- 
filtrations are  commonly  present  in  the  tissues  at  the  base  of 
inflamed  valves,  and  are  also  widely  disseminated  tliroughout 
the  heart.  Bacteria  have  not  hitherto  been  found  in  them. 
As  regards  their  ultimate  fate,  the  smaller  nodules  may  be 
completely  absorbed,  but  the  larger  lesions  persist. 

Myocardial  nodules  are  not  confined  to  cases  of  acute 
rheumatism,  and  have  been  found  in  many  varieties  of  acute, 
infection   (pneumonia,   pleurisy,   smallpox,   blackwater  fever 


24  :  \        DISEASES  OF  THE  HEART 

enteric  feveTy  sepsis,  diphtheria,  scarlatina,  chorea,  leukaemia ). 
The  indiYidual  lesion  is  minute  and.  of  comparatively  Httle 
importance,  but  their  situation,  or  numbers  may  produce  con- 
siderable'interference  with  the  proper  working  of  the  heart, 
both  in  the  acute  and  in  the. chronic  stages.  The  heart,  it 
must  be  remembered,  cannot  be  immobilized  like  a  broken 
leg,  and  its  constant  movement  produces  a  "callus  "  quite 
out  of  proportion  to  the  original  lesion. 

Periarterial  fibrosis  must  be  sharply  differentiated  from 
the  para-arterial  form.  The  latter  is  dystrophic,  and  the 
result  of  coronary  narrowing ;  while  the  former  is  inflammatory 
in  nature. 

The  Mixed  Form  of  Fibrosis. — Para-arterial  and  peri- 
arterial fibrosis  may  occur  as  individual  lesions,  but,  in  perhaps 
the  majority  of  cases  of  fibrosis,  occur  together,  though  the 
amount  of  each  kind  varies.  This  is  the  necessary  result  of 
the  arterial  causes.  Endarteritis  may,  it  is  true,  be  the  sole 
lesion  in  an  artery,  but  in  all  extreme  cases  the  other  coats 
are  also  involved ;  and  in  adventitial  lesions  the  vasa  yasorum 
are  often  affected  and  intimal  changes  ensue,  so  that  fre- 
quently intimal  and  adventitial  lesions  coincide,  and  both 
forms  of  fibrosis  coexist. 

The  special  localization  of  cardiac  fibrosis  is  due  to  the 
frequency  with  which  it  is  dependent  upon  coronary  disease, 
Huchard  has  pointed  out  that  the  left  coronarj^  artery,  its 
descending  branch  in  particular,  is  much  more  frequently 
abnormal  than  the  right.  The  work  which  it  has  to  perform 
is  greater,  extra  strain  is  more  frequently  imposed  upon  it, 
and  it  divides  rapidly  into  many  branches.  The  right  artery, 
too,  in  its  bed  of  fat  in  the  auriculo-ventricular  sulcus,  is 
much  better  protected  and  much  less  strained  during  the 
cardiac  contractions.  The  arteries  of  the  musculi  papillares 
are  the  longest  branches  of  the  system,  and  have  a  course 
which  is  particularly  tortuous,  and  are,  in  consequence,  likely 
to  suffer  in  any  disadvantageous  circumstance. 

Another  factor,  a  local  spread  of  inflammation  from  the 
auriculo-ventricular  valve,  may  also  be  active  in  the  case  of 
the  musculi  papiUares,  for,  in  all  marked  cases  of  mitral  disease 
the  papillae  are  sclerosed,  the  fibrosis  being  most  extreme  at 


THE  DISEASES  OF  THE  MYOCARDIUM 


25 


tlie  tip,  and  the  chordae  are  thickened  and  shortened.  So 
that,  although  the  anatomical  peculiarity  of  their  blood- 
supply  is  in  itself  sufficient  to  explain  the  special  frequency 


Fig.  17. — Gumma  of  Heart. 
(From  a  water-colour  drawing  by  Dr.  Ales  Macphail,  W.  I.  Mus.) 

with  which  they  are  diseased,  another  factor  inflammatory  in 
origin  assists  to  make  the  pre-eminence  still  more  marked. 

The  other  possible  causes  of  fibrosis  are  of  comparatively 
Httle  importance. 


26  DISEASES  OF  THE  HEART 

Hcemorrhages  are  not  infrequently  found  post-mortem. 
They  are  generally  subpericardial,  but  also  occur  beneath  the 
endocardium  and  in  the  substance  of  the  muscle.  They  are 
usually  small  and  cause  little  damage  to  the  muscle,  but  are 
occasionally  large,  and  the  muscle  in  their  vicinity  is  degenerate. 
In  such  cases  death  as  a  rule  occurs  early,  but  if  recovery  takes 
place,  scar  formation  may  conceivably  result. 

Tumours  and  tubercular  masses  in  the  cardiac  waU  are  rare, 
and  are  usually  secondary ;  hydatid  cysts  have  been  occasionally 


Fig.  18. — Fibrosis  of  the  Myocardium,     ^x  50.) 
(From  a  case  of  syphilis  during  the  secondary  stage.) 

found ;  and  all  these  lesions  occasion  fibrosis  in  their  vicinity. 
Wotmds  of  the  heart  and  trauma  (Pleasants),  even  without 
actual  penetration,  may  lead  to  scar  formation. 

Syphilitic  lesio7is  may  be  met  with.  The  most  important 
is  specific  endarteritis  of  the  coronar}?^  arteries,  whose  lumen 
may  be  narrowed  or  occluded,  in  which  case  a  dystrophic 
fibrosis  results  (Fig.  10).  Gummata  (Fig.  17)  have  been 
found  in  a  not  inconsiderable  number  of  cases,  and  maj^  con- 
ceivably be  responsible  for  some  mj^ccardial  scars;  and  a 
diffuse  periarterial  fibrosis  (Fig.  18)  is  recognized  as  occurring 


THE  DISEASES  OF  THE  MYOCARDIUM 


27 


during  the  secondary  stages  of  the  acquired  disease,  and  in 
congenital  infections.* 

Fibrosis  of  the  heart  may  thus  be  due  to  several  causes. 
In  the  great  majorit}-  of  cases,  and  in  all  examples  of  gross 
disease,  it  is  the  result  of  ischsemic  destruction  of  the  muscle 


Fig.  19. — Infakct  of  a  Papillahy  Muscle,  with  Rupture,  from  Disease  of 
THE  Coronary  Arteries.     (R.  I.  Mus.)  j  ^ 

cells,  following  obstruction  of  the  coronar}^  arteries  and  second- 
ary connective-tissue  hyperplasia.  In  other  cases  the  fibrosis 
Kes  around  the  arterioles,  and  is  a  primary  connective-tissue 
reaction.     These  two  forms  often  coexist. 

Fibroid  patches  may  be  due  to  mural  endocarditis,  but  the 
lesions  are  never  large ;  they  are  rarely,  if  ever,  due  to  pericarditis . 
*  Wartliin,  Amer.  Journ.  Med.  Sci.,  1911,  vol.  cxli.,  p,  398. 


28  DISEASES  OF  THE  HEART 

S}T3liilis  and  trauma  very  occasionally  produce  scars. 

Chronic  valvular  disease  seems  alwaj^s  to  be  accompanied 
by  some  degree  of  fibrosis  which  is  most  extreme  in  the  vicinity 
of  the  affected  valve,  though  it  also  occurs  throughout  the 
heart  in  lesser  degree. 

Hypertrophied  hearts  are  not  necessarily  fibroid,  though 
this  frequently  obtains  from  associated  arterial  disease. 

Aneurism  of  the  Heart  is  comparatively  rare.  It  may  be 
situated  anywhere,  but  is  most  common  in  the  lower  part  of 
the  left  ventricle.  The  right  ventricle  is  seldom  imphcated, 
and  the  auricles  still  less  frequently.  The  aneurism  may  be 
of  any  size,  and  is  sometimes  as  large  as  an  orange. 

Aneurism  is  always  secondary  to  myocardial  lesions,  which 
so  weaken  the  wall  that  the  intracardiac  pressure  causes 
bulging.  The  myocardial  lesions  may  be  of  various  kinds. 
An  acute  mural  endocarditis  is  occasionally  the  cause,  and 
usually  involves  the  septum.  Myomalacia  and  dystrophic  | 
fibrosis  are  more  common,  and  most  frequently  affect  the' 
lower  part  of  the  left  ventricle.  A  traumatic  scar,  the  result 
of  a  stab  ten  years  before  death,  has  been  followed  by  the 
formation  of  an  aneurism. 

In  the  majority  of  cases  the  wall  is  fibroid  and  greatly 
thinned,  being  sometimes  only  a  fourth  of  the  normal  thick- 
ness. The  endocardium  is  thickened  and  opaque,  and  often 
Hned  by  laminated  clot.  The  visceral  pericardium  is  thickened 
and  frequently  adherent  to  its  parietal  layer.  The  bulk  of 
the  muscle  has  disappeared,  though  a  few  cells  may  persist 
beneath  the  endocardium  and  the  pericardium. 

Rupture  o£  the  Heart  is  most  frequently  due  to  myomalacia 
the  result  of  coronary  occlusion.  If  an  infarct  occurs  and 
the  patient  survives,  an  inflammatory  reaction  takes  place  in 
the  periphery  of  the  necrotic  area,  with  resultant  weakening  of 
the  tissues.  If  it  extends  near  the  endocardium,  the  endo- 
cardial blood  soon  forces  an  entrance,  and  tearing  its  way 
along  the  track  of  the  softening  with  each  successive  heart-beat, 
it  ultimately  reaches  and  perforates  the  pericardium.  The 
path  of  the  blood  may  thus  be  devious,  and  the  endocardial 


THE  DISEASES  OF  THE  MYOCARDIUM  29 

and  pericardial  lacerations   may  not  correspond  unless   the 
communication  is  large. 

Rupture  may  also  occur  from  trauma,  intramural  abscess, 
and  aneurism. 


EEFEEENCES. 
John  Cowan: 

On  Obstruction  of  the  Coronary  Arteries.     Trans.  Path,  and  Clin.  Soc, 

Glasgow,  1902,  vol.  ix.,  p.  49. 

Fatty  Degeneration  of  the  Myocardium.    Joum.  of  Path.,  London,  1903, 

vol.  viii.,  p.  177. 

The  Heart  in  Acute  Disease.     Ihid.,  1904,  vol.  ix.,  p.  87. 

The  Fibroses  of  the  Heart.     Ihid.,  1904,  vol.  ix.,  p.  209. 

Cakey  Coombs: 

Submiliary  Nodules  of  Acute  Rheumatic  Carditis.    Ihid.,  1911,  vol.  xv., 

p.  489. 

The  Histology  of  Experimental  Rheumatism.     Lancet,  London,  1912, 

vol.  ii.,  p.  1209. 

Louis  Gallavardin:  La  Degenerescence  Graisseuse  du  Myocarde.     These 

de  Paris,  1900. 

Rene  Marie:  L'Infarctus  du  Myocarde.     These  de  Paris,  1896. 


CHAPTER  II 

THE  DISEASES  OF  THE  ARTERIES 

The  Arteries. — It  has  been  customary  to  consider  the  arterial 
wall  as  composed  of  three  layers — the  intima,  the  media,  and 
the  adventitia ;  but  while  this  is  useful  from  the  descriptive 
point  of  view,  it  tends  to  produce  the  idea  that,  physiologi- 
cally, the  layers  are  distinct  and  separate,  an  idea  which  is 
essentially  inaccurate.     The  internal  elastic  lamina,  it  is  true, 
in  the  smaller  vessels   marks  abruptly  the  line  of  division 
between  intima  and  media,  but  it  is  absent  in  the  aorta  and 
the  larger  arteries,  and  the  precise  limits  of  the  layers  are,  in 
consequence,    indefinite.     Muscular    fibres    are    not    confined 
to  the  media  alone,  but  are  present  in  both  the  intima  and 
the  adventitia;  and  though  they  are  in  the  smaller  vessels 
the  main  constituent  of  the  middle  layer,  in  the  larger  trunks 
they  are  relatively  scanty,  and  the  elastic  tissue  is  the  essential 
element.     The  two  groups  of  vessels  must  be  sharply  separated. 
One  group  are  the  "  mains  "  for  the  supply  of  blood  to  the 
tissues,  with  a  calibre  proportionate  to  the  amount  of  blood 
which  they  have  to  accommodate,  and  a  structure  adapted  to 
resist  the  varying  degrees  of  blood-pressure  to  which  they  are 
exposed.     The    other    group    are    the    "  supply-pipes  "    with 
"taps,"  which  can  be  partially  closed  and  so  rearrange  the 
distribution  of  the  blood  to  the  different  viscera.     The  adven- 
titia is  but  a  part  of  the  general  connective  tissue,  and  can 
seldom  be  exactly  demarcated,  and  the  connective  tissue  and 
the  elastic  framework  of  the  three  layers  are  structurally  in 
contact.     The   essential  constituent   of   the   bloodvessels,   as 
the  late  Professor  Coats  maintained,  is  the  intimal  pavement 
endothelium. 

The  relations  of  the  three  layers  may  vary  even  in  the  same 

30 


THE  DISEASES  OF  THE  ARTERIES  31 

artery  in  different  portions  of  its  course.  Particular  parts 
may  be  exposed  to  special  stress,  and  the  liability  to  local 
damage  is  to  a  certain  extent  compensated.  The  upper  wall 
of  the  ascending  aortic  arch,  exposed  to  the  full  force  of  the 
ventricular  systole,  is  much  thicker  than  the  opposite  side, 
where  the  systolic  impact  is  less  direct,  and  vessels  are  always 
thickened  at  bifurcations  and  around  the  origins  of  branches 
to  meet  the  extra  strain.  Arteries  such  as  the  facial  superior 
mesenteric  and  brachial  are  exposed  to  injury  from  the 
movements  of  the  neighbouring  parts,  and  possess,  in  conse- 
quence, an  adventitia  which  is  notably  thick;  while  others 
such  as  the  abdominal  aorta  and  the  nutrient  arteries  of  the 
bones  are  protected  from  such  influences  by  their  situation, 
and  have  an  adventitia  of  little  thickness.  The  relative 
proportion  of  the  different  elements  of  each  layer  varies  in 
different  vessels  of  similar  size.  The  media  of  the  renal 
arteries,  for  example,  contains  a  much  larger  proportion  of 
muscle,  and  a  much  smaller  amount  of  elastic  tissue  than  such 
a  vessel  as  the  carotid;  and  one  cannot  predicate  what  the 
exact  constitution  of  an  artery  will  be,  since  the  individual 
elements  may  var}^  in  amount  from  its  special  function  or  its 
special  site. 

The  vascular  arrangements  of  the  arterial  wall  point  the 
same  moral.  The  nutrition  of  the  vessel  is  maintained  by 
two  sources.  The  vasa  of  the  adventitia  penetrate  for  a 
certain  distance  into  the  media  of  the  larger  arteries,  but  under 
normal  circumstances  do  not  trespass  far.  The  minute 
vessels  have  no  vasa,  and  must  be  largely  dependent  upon  the 
blood  within  them,  although  no  definite  lymphatic  connection 
is  apparent.  It  is  difficult  to  estimate  how  much  of  the  wall 
is  supphed  from  each  source,  but  in  endarteritis  the  cells 
nearest  the  blood-stream  are  always  less  degenerate  than 
those  farther  away;  and  in  some  cases  of  medial  fibrosis  the 
innermost  muscle  cells  persist,  while  those  in  the  centre  of  the 
layer  have  disappeared  (Fig.  21);  so  that  it  seems  clear  that 
in  abnormal  circumstances  both  media  and  intima  may  be 
nourished  by  the  intra-arterial  blood.  All  the  muscle  cells 
of  the  media,  however,  may  be  intact  in  cases  of  endarteritis, 
and  the  vasa  are  sometimes  seen  to  penetrate  into  the  intima. 


32  DISEASES  OF  THE  HEART 

so  that  both  layers  may  at  times  be  supphed  from  without. 
It  seems  probable  that  normally  the  medial  source  is  mainly 
vasal,  and  the  intimal  source  mainly  intra-arterial,  while 
under  abnormal  conditions  a  defect  in  one  supply  can  be 
more  or  less  compensated  by  the  other.  New-formed  blood- 
vessels in  the  media  and  the  intima  are,  however,  always 
branches  of  the  vasa. 

Lymphatic  flow  takes  place  from  within  outwards,  although 
no  definite  lymph  channels  are  present  in  the  vessel  wall. 
But  in  early  cases  of  endarteritis  the  muscle  cells  in  the  vicinity 
of  the  degenerate  intima  are  not  infrequently  fatty,  as  the 
result  of  the  local  toxsemia. 

The  functional  and  structural  arrangements  of  the  arterial 
wall  thus  necessarily  entail  some  damage  to  more  than  one 
layer  in  all  but  the  very  slightest  lesions.  In  advanced  cases 
all  the  layers  are  ahnormal,  though  the  degree  to  which  each 
is  involved  may  vary,  and  this  occurs  quite  irrespective  of  the 
site  of  the  initial  lesion. 

A  clear  distinction  must  be  drawn  between  the  two  main 
groups  of  arterial  disease:  (l).The  di-ffuse  form,  and  (2)  the 
focal  or  nodidar  lesions ;  for  the  causes  and  the  results  of  the 
two  are  notably  different.  The  second  group  comprises 
atheroma,  patchy  mesarteritis,  endarteritis  obliterans,  and 
medial  calcification;  the  first  arterio-sclerosis,  using  the  term 
in  its  more  restricted  sense. 

Arterio-Sclerosis. — Arterio-sclerosis  is  a  diffuse  affection, 
and  all  the  arteries  and  capillaries,  and,  according  to  some 
writers,  the  veins  as  weU,  are  abnormal.  The  lesions  are  best 
marked  in  the  smaller  vessels  whose  walls  are  distinctly  and 
uniformly  thickened.  The  medium-sized  arteries  (renal,  etc.) 
are  also  thickened,  and  their  consistence  may  be  firmer  than 
normal.  The  aorta  is  thickened  generally,  and,  in  addition, 
in  old-standing  cases  shows  many  atheromatous  patches.  In 
th^  early  stages  the  resilience  of  the  vessels  may  be  good,  but 
in  advanced  cases  is  distinctly  impaired. 

Microscopic  examination  shows  alterations  in  all  the  three 
layers.     The  intima  is  usually  more  or  less  thickened  (Fig.  20), 


THE  DISEASES  OF  THE  ARTERIES  33 

There  is  always  great  hypertrophy  of  the  elastic  fibrils,  and 
two  or  more  laminae,  sometimes  of  considerable  thickness, 
may  be  evident.  In  older  cases  degenerative  changes  are 
present,  the  elastic  tissue  becoming  granular  and  the  connective 
tissue  hyahne  and  sparsely  nucleated,  but  the  gross  fatty  and 
calcareous  deposits,  which  are  met  with  in  atheroma,  are 
rarely,  if  ever,  seen.     The  media  is  always  abnormal.     In  early 


Fig.  20. — Arteeio-Sclerosis:  Elastic  Tissue  stained  to  show  the 
Hyperplasia  ik  the  Intima.     (x  75.) 

cases  it  is  thicker  than  usual,  but  the  relative  proportions  of 
muscle,  elastic  and  connective  tissue,  are  preserved,  the  only 
alteration  being  the  hypertrophy.  In  other  cases  it  may  be 
thinned,  the  muscle  ceUs  being  atrophied  and  perhaps  fatty; 
while  in  a  third  group  the  connective  and  elastic  elements 
are  in  excess  and  the  muscle  cells  are  degenerate  and  few  in 
number,  in  advanced  cases  only  persisting  along  the  edges  of 
the  coat  (Fig.  21).     They  are  most  numerous  and  least  altered 

3 


34 


DISEASES  OE  THE  HEART 


along  the  outer  margin,  but  may  persist  along  the  inner  edge, 
while  those  in  the  centre  have  disappeared.  The  connective 
tissue  is  usually  hj^ahne  or  granular,  and  sparsely  nucleated; 
and  the  elastic  fibrils,  though  excessive  in  number,  are 
degenerate  and  granular  (Fig.  22).  The  adventitial  changes  are 
less  variable.     The  outer  coat  is  almost  invariablv  thickened, 


Fig.  21. — Aeteeio-Scleeosis.     (xoO.) 
The  media  is  fibroid,  and  only  a  few  muscle  cells  persist  along  the  margins. 

being  in  the  early  stages  thickly  nucleated,  and  in  old-standing 
cases  hyahne  and  sparsely  nucleated.  The  elastic  tissue, 
here  as  elsewhere,  is  always  excessive. 

The  adventitial  thickening  is  the  onl}^  constant  change  in 
these  cases.  If  the  media  is  thickened  or  fibroid,  the  intima 
may  be  but  little  abnormal;  but  if  the  former  is  atrophied,  the 
latter  is  generally  hj^ertrophied.  WiUiam  Russell  states 
that  the  changes  in  the  intrarenal  vessels  tend  to  intimal 
thickening,  while  the  medial  hypertrophy  is  best  marked  in 


THE  DISEASES  OF  THE  ARTERIES 


35 


the  extrarenal  vessels ;  but  this  may  be  due  to  the  renal  lesion 
being  of  older  date.  There  has  been  considerable  discussion 
in  the  past  as  to  the  precise  histological  details  of  the  arterial 
lesions.  But  it  is  now  generally  agreed  that  medial  hyper- 
trophy   (hypermyotrophy)   is   an  early  and  essential  phase 


Fig.  22. — Akteeio-Sclerosis.     (x  75.) 

The  same  vessel  as  Fig.  21,  stained  to  show  the  degenerate  new-formed  elastic 

fibres. 


that  it  occurs  throughout  the  whole  arterial  system,  and  that 
fibroid  changes  supervene  both  here  and  in  the  adventitia 
•at  a  comparatively  early  period. 

The  capillary  vessels  are  also  abnormal.  A  healthy  capillary 
•cut  transversely  is  apt  to  escape  observation,  the  waU  being 
■8b  mere  hair-hne;  but  in  the  cases  which  we  are  considering, 
•a  double  contour  is  usually  visible,  the  wall  being  several 
times  its  usual  thickness;  the  lumen,  too,  may  be  somewhat 
iiarrow^d. 


36 


DISEASES  OF  THE  HEART 


It  has  been  known  for  long  that  the  blood-pressure  in  cases 
of  cirrhotic  kidney  is  almost  always  elevated,  sometimes  to 
an  extraordinary  degree ;  and  it  was  at  first  supposed  that  this 
was  due  to  the  associated  arterial  disease.  In  1903,  how- 
ever, Sir  Clifford  AUbutt  published  a  paper,*  in  which  he 
urged  that  arterial  disease  was  not  the  cause  of  an  elevated 
blood-pressui^e,  but  rather  its  result.  "The  pressure  may 
be,  and  often  is,  low  throughout  the  course  of  arterial  degenera- 
tion; or,  again,  having  been  high,  it  may  fall;  though,  of 
course,  in  some  elderty  persons  with  arterial  decay,  occasional 
transient  attacks  of  high  pressure,  such  as  occur  at  times  in  all 

of  us,  maj'  be  observed."  Con- 
versely, high  blood-pressure  can- 
not be  maintained  for  long 
without  arterial  strain;  and 
arteriosclerosis  results  from  long 
persisting  high  Mood- 'pressure  of 
tvhatsoever  origin. 

The  process  is  well  seen  in  cases 
of  nephritis.  In  acute  nephritis 
the  blood-pressure  is  almost  in- 
variabh^  elevated  in  the  presence 
of  symptoms  and  falls  with  their 
remission,  reaching  normal  read- 
ings in  the  majoritj^  of  cases  long 
before  the  albuminuria  disappears. 
In  the  chronic  forms  of  nephritis 
the  blood-pressure  is  not  invariably  elevated,  and  is,  indeed, 
as  a  rule  low  in  cases  of  large  white  kidney  (Fig.  23),  but  it 
is  always  high  in  contracted  kidneys  (Fig.  24),  whether  these 
are  primary  or  foUow  an  acute  attack.  In  cirrhotic  kidney, 
as  Dickinson  has  shown,  the  whole  of  the  arterial  tree  is 
affected,  and  the  walls  of  the  aorta  and  the  great  vessels,  as 
well  as  the  smaller  branches,  are  notably  thickened. 

The  elevation  of  pressure  in  these  cases  si  due  to  an  increase 
in  the  peripheral  resistance,  which  can  only  result  from  one 
of  two  causes :  a  diminution  in  the  calibre  of  the  vessels,  or  an 
increased  viscosity  of  the  blood.     Arterial  disease  does  in  many 

*  Lizncet,  1903,  vol.  i.,  pp.  170,  329,  472,  645, 


MAR  APR  MAy  JUN  JUL  AUG  SEP 


mm 

140 

130 

120 

no 
«oo 

90 
80 

70 

Fig.    23. — Blo  od-Peesstjee 
Chaet. 

M„  aged  23.  Large  white  kidneys 
weighing  16  ounces.  The  heart 
weighed  6J  ounces. 


28 

25 

24 

9 

28 

2Q 

22 

y 

/N 

V 

>r^ 

>^ 

N 

v- 

^ 

A 

^ 

/ 

THE  DISEASES  OF  THE  ARTERIES 


37 


cases  narrow  the  lumen,  but  it  also  'sometimes  widens  it; 
■and  if  it  lessens  it  in  some  places,  the  local  narrowing  may 
be  compensated  by  dilatation  elsewhere.  In  syphilitic  disease 
•of  the  arteries,  the  lumen  is  often  greatly  narrowed,  though 
the  blood-pressure  may  never  be  above  the  normal. 

The  second  factor,  increased  viscosity  of  the  blood,  may 
■conceivably  be  active  in  certain  cases,  but  accurate  observa- 
tions on  this  point  are  difficult  to  obtain,  for  the  methods  of 
estimation  are  not  above  suspicion  even  in 
laboratory  experiments,  and  many  diverse 
factors  which  may  influence  it,  but  cannot 
be  accurately  measured,  come  into  opera- 
tion in  the  wards.  The  viscosity  of  the 
whole  blood  rises  steadily  during  the  period 
of  growth,  and  is  higher  in  men  than  in 
women.  It  is  affected  by  menstruation  and 
pregnancy,  by  sweating  exercise,  by  alti- 
tude, by  variations  in  the  red-ceU  and  the 
white-cell  counts,  and  by  the  percentage  of 
oxygen  and  of  carbonic  acid  in  the  blood, 
as  well  as  by  the  saline  and  the  colloid  con- 
tent ;  while  it  has  no  constant  relation  to 
the  specific  gravity  of  the  blood  or  the 
height  of  the  blood-pressure.* 

The  viscosity  is  almost  always  increased 
in  polycythsemia,  and  Parkes  Weberf  and 
others  have  shown  that  it  may  be  twice  Fig.  24.— Blood-Pbes- 
or  thrice,  or  even  four  times,  greater  than  ^"^^^  Chart, 

normal  in  cases  of  erythremia,  in  which  \Xeyt  wfjhtg"i2| 
disease    the    blood-pressure  is  usually  in- 
creased,   apparently   in    consequence;    for 
although  this  might  be  due  to  renal  disease,  which  is  a  common 
accompaniment  in  these  cases,  the  kidneys  may  be  normal, 
as    in   Case    21    of   Weber's    series,  in  which  the  heart   was 
"somewhat  hypertrophied." 
In  one  group,  the  polyoythcenla  hypzrtonica  of  Grsisbock  and 

*  Sir  CiiEfjrd  Allbitfc,  Q  ixrl.  Joitrn,.  of  MiL,  1310-11,   vol.riv.,   p.   342. 
W.  H.  Welsh:  '  He%rt;  1911-12,  vol,  iii.,  p.  118. 
t  Qmrt.  Journ.  of  Med.,  1908-09,  vol.  ii.,"p.  85. 


9 

10 

V 

,, 

Sr^ 

^ 

as 

N» 

NOV 


Hg. 
mm 

210 


190 
ISO 
170 
160 
150 
140 
130 
120 
110 
100 
90 
80 
70 


ouaces.      The    heart 
weighed  18  ouaces. 


38  DISEASES  OF  THE  HEART 

Hess,  the  same  relationship  apparently  obtains.  I  have  seerc 
one  case  of  this  kind. 

The  patient,  a  solicitor  aged  thirty-nine,  had  been  steadily 
losing  strength  and  flesh  for  at  least  a  jesbT,  and  had  been, 
noticed  to  be  "  blue  "  in  colour  for  the  same  time.  He  had 
had  several  attacks  of  "influenza,"  in  which  he  was  fevered, 
and  shivered  frequently,  and  experienced  very  severe  head- 
ache, while  there  was  but  little  catarrh;  and  during  these 
illnesses  he  became  notably  c^^anosed,  while  his  urine  con- 
tained much  albumin.  He  was  a  well-built  but  badly 
nourished  man,  and  sweated  profusely.  The  cyanosis  was 
always  considerable,  and  once  when  I  saw  him  during  cold 
weather  extraordinary  in  its  degree,  and,  although  general,. 
much  more  intense  in  the  head  and  neck  than  elsewhere.  The 
jugular  veins  were  turgid  and  prominent.  The  heart  was 
shghtly  enlarged,  the  second  aortic  sound  loud  and  ringing, 
and  the  peripheral  arteries  thick  and  tortuous.  The  retinal 
arteries  were  of  characteristic  silver  wire  appearance.  The 
brachial  systohc  pressure  measured  175  to  180  mm.  Hg. 
The  hver  and  spleen  were  shghtly  enlarged,  and  the  urine 
habituafly  contained  albumm  in  varying  amount,  sometimes,, 
however,  only  a  trace.  The  red  cells  numbered  10,000,000, 
the  haemoglobin  value  was  120  per  cent.,  and  the  white  ceUs- 
numbered  22,400  per  c. mm.  The  average  size  of  red  cell  wa& 
rather  above  the  normal,  and  a  few  cells  were  certainly 
megalocytes.  No  erythroblasts  were  seen.  The  white  cells 
were  chiefly  polymorphonuclear. 

The  patient  himself  was  definite  that  his  illness  had  lasted 
for  some  twenty  years,  though  it  was  only  recently  that  he- 
had  been  seriously  inconvenienced;  and  he  had  conducted  a 
considerable  business  during  this  period.  He  was  a  married 
man  with  a  healthy  family.  He  had  alwaj^s  been  liable  tO' 
bilious  headaches,  even  as  a  boy  at  school,  and  these  had 
gradually  become  more  severe  and  of  longer  duration.  They 
recurred  every  few  weeks,  and  his  tongue  became  coated  and 
his  bowels  confined  during  their  persistence.  He  was,  he 
said,  a  "fair"  hoj,  but  his  complexion  darkened  in  the 
twenties,  and  in  the  early  thirties  he  became  "plethoric." 
His  father,  too,  had  been  "blue  "  for  the  last  twenly  years 


THE  DISEASES  OF  THE  ARTERIES  39 

of  his  Life;  but  he  had  carried  on  business  until  shortly  before 
his  death  at  the  age  of  seventy,  after  an  iUness  of  ten  days' 
dui'ation. 

This  patient  died  about  two  years  after  I  first  saw  him, 
and  there  was  no  post-mortem  examination,  so  that  the  con- 
dition of  his  kidneys  was  not  ascertained.  But  it  seems 
probable  that  the  polycythaemia  was  the  primary  event  and 
the  cause  of  the  increased  blood  -  pressure  and  the  cardio- 
vascular hypertroph}". 

There  has  been  some  difference  of  opinion  as  to  the  site  of 
the  increased  peripheral  resistance.  Sir  Chfforcl  thinks  that 
it  is  in  the  capiUary  network  as  in  normal  individuals,  while 
Sir  Douglas  PoweU,  Russell,  and  others  maintain  that  it  is 
situated  in  the  finer  arterioles.  Broadbent  and  Sansom 
thought  that  both  factors  might  be  active.  The  last  opinion 
seems  probably  correct,  for  although  the  first  theory  seems 
applicable  to  the  polj^cythaemic  group,  vasodilator  drugs 
can  often  in  other  cases  relieve  high  pressure,  at  any  rate 
temporarity,  and  their  action  can  only  influence  the  muscular 
arterioles . 

The  blood-pressure  in  elderly  persons  may  be  elevated 
without  any  evidence  of  renal  lesions  (hyperpiesis),  and  Sir 
Chfford  thinks  that  the  most  important  cause  is  "repletion, 
relative  or  absolute — i.e.,  tempered  or  untempered  by  air  and 
exercise."  Although  at  first  the  elevation  may  disappear  as 
the  result  of  suitable  treatment,  it  tends  as  a  rule  to  recur 
and  to  become  permanent,  and  to  be  ultimately  associated 
with  arterial  thickening.  WilHam  Russell  has  also  brought 
forward  evidence  in  support  of  the  same  theory.  He  differs 
from  Sir  Chfford  in  his  contention  that  the  initial  error  is 
always  an  excessive  ingestion  of  food  greater  than  the  work 
done  requires  or  ehmination  can  overtake;  and  suggests  that 
in  many  cases  the  chief  cause  is  an  intoxication  due  to  gastro- 
intestinal indigestion  and  the  production  of  hypertonic 
substances.  There  seems  to  be  little  doubt  that  both  ob- 
servers have  right  on  their  side,  but  it  seems  certain  that  other 
causes  may  also  be  active,   for  the  association  of  gout  and 


40  DISEASES  OF  THE  HEART 

chronic  lead-poisoning  with  arterio-sclerosis  has  been  recog- 
nized for  long,  though  the  precise  mechanism  by  which  the 
blood-pressure  is  elevated  is  still  undetermined.  Renal  disease, 
in  these  cases,  though  commonly  present,  may  be  absent, 
though  the  arterial  lesions  are  well  marked. 

The  isolation  of  adrencilin  and  the  discover}^  by  Josue  of 
its  action  in  producing  arterial  disease  in  rabbits  have  focussed 
the  attention  of  man}^  observers  upon  the  suprarenal  capsules, 
and  it  has  been  demonstrated  that  these  bodies  are  very  often 
enlarged  both  in  chronic  renal  disease  and  in  cases  of  arterial 
disease.  The  chief  alterations  which  have  been  described 
have,  however,  been  situated  in  the  cortical  parts  of  these 
organs,  while  it  is  known  that  adrenahn  is  the  product  of  the 
medulla ;  but  Josue  has  shown  that  substances  obtained  from 
the  cortex,  though  not  adrenahn,  have  also  a  hypertonic  action 
upon  the  vessels,  and  maintains  that  cortical  hj^perplasia, 
however  it  may  act,  whether  by  some  reaction  preparatory 
to  the  secretion  of  adrenalin  by  the  meduUa,  or  by  its  own 
effects,  is  an  index  to  the  activity  of  the  gland  as  a  whole. 

Thayer*  has  pointed  out  that  the  blood-pressure  is  often 
elevated  following  an  attack  of  enteric  fever,  and  states  that 
the  average  systolic  pressure  in  such  individuals  is  appreciably 
higher  than  that  of  healthy  individuals  of  the  same  age,  and 
that  the  radial  arteries  are  palpable  nearly  three  times  as 
often  as  they  are  in  health}^  persons  who  have  never  had  the 
disease.  It  is  difficult  to  understand  vihj  this  should  occur, 
as  the  blood-pressure  during  an  attack  is  low,  and  tends  to 
fall  rather  than  to  rise.  The  small  arteries,  however,  are  not 
infrequently  affected  in  the  acute  infections  [vide  p.  48),  and 
the  lesions  are  often  associated  with  microscopic  damage  to 
the  viscera  (submiliary  nodules  in  the  heart,  focal  necrosis 
in  the  liver,  cellular  collections  in  the  kidneys,  etc.),  and 
although  the  separate  lesions  are  individually  negligible, 
their  collective  result  in  cases  where  they  are  "wddespread  may 
be  considerable,  and  may  lead  to  such  an  increas^e  of  the 
peripheral  resistance  that  an  elevation  of  the  blood-pressure 
is  produced. 

*  Amer.  Journ.  Med.  Set.,  1904,  vol.  cxxvii.,  p.  391 ;  Johns  Hopkins  Hosp. 
Bull,  1904,  vol.  XV.,  p.  323. 


THE  DISEASES  OF  THE  ARTERIES  41 

Hypertrophy  of  the  media,  and  probably  of  the  adventitia 
as  well,  ensues  as  the  natural  sequel  of  the  increased  work 
imposed  upon  the  vessels,  but  there  is  a  very  fine  distinction 
Ibetween  the  degree  which  induces  hypertrophy  and  that 
which  initiates  degenerative  changes;  and  "sooner  or  later 
the  body  meets  with  circumstances  in  which  either  the  nutri- 
tion is  not  maintained,  or  the  stimuli  acting  on  the  media 
hecome  greater  than  can  be  sustained  "  (Klotz),  and  degenera- 
tive changes  ensue  with  atrophy  of  the  "noble"  muscular 
•cells,  and  hypertrophy  of  the  less  highly  speciahzed  connective 
tissue  according  to  the  usual  rules.  The  causes  of  the  in- 
timal  thickening,  when  it  occurs,  may  be  similar,  or  it  may 
I)e  due  to  continued  irritation  by  toxic  materials  in  the  blood- 
stream. 

2.  The  Focal  Lesions — Atheroma  {Endarteritis  nodosa  vel  defor- 
mans).— Atheromatous  patches  are  almost  invariably  present  in 
the  arteries  of  elderly  persons,  though,  of  course,  their  number, 
.«ize,  and  distribution  vary  in  different  cases.  The  patches  are 
■elevated  above  the  surface  with  more  or  less  abrupt  edges,  and 
<even  in  small  vessels  rarely  involve  the  whole  circumference. 
Sometimes  they  are  mere  pin-points,  sometimes  plaques  as 
large  as  a  shilling,  and  they  may,  by  coalescence,  involve 
■comparatively  large  areas.  In  the  early  stages  th.ey  are  soft 
and  gelatinous  and  translucent;  in  the  later  stages  opaque 
And  fu-m,  or  hardened  by  calcareous  deposits.  Ulceration 
is  not  uncommon,  and  thrombi  may  be  deposited  upon 
them. 

It  is  generally  agreed  that  the  first  portions  of  the  aorta  are 
axLost  often  involved,  but  there  is  a  difference  of  opinion  as  to 
the  frequency  with  which  the  other  arteries  are  affected, 
'  The  coronary  arteries  of  the  heart,  the  cerebral  and  the 
peripheral  arteries,  are,  however,  affected  more  often  than 
those  of  the  abdominal  viscera,  and  the  pulmonary  arteries  are 
but  seldom  damaged,  save  in  cases  of  clironic  pulmonary  or 
cardiac  valvular  disease. 

The  early  lesions  are  found  in  the  deeper  layers  of  the  intima 
(Fig.  25),  but  in  advanced  examples  the  whole  thickness  of 
the  wall  is  found,  on  microscopic  examination,  to  be  involved, 
though  the  degree  to   which  each  layer  is  affected  varies  in 


42  DISEASES  OF  THE  HEART 

different  cases.  The  intima  is  always  thickened,  often  greatly^ 
and  in  the  early  stages  is  very  cellular,  the  elastic  tissue- 
sharing  in  the  hj^erplasia.  In  the  later  stages  degeneration 
occurs,  and  fatty,  granular,  mucoid,  hyahne,  or  calcareous 
changes  may  be  found,  always  most  extreme  near,  though  not 
necessarih"  next,  to  the  outer  margin  of  the  coat.     The  media- 


FiG.  25.— Early  Atheroma,     (x  40.) 
The  intima  alone  is  thickened;    elastic  stain. 

is  atrophied  often  to  a  notable  degree,  and  may  be  entirely'' 
destroj^ed,  and  its  elastic  tissue  may  be  excessive  and  de- 
generate. The  adventitia  as  a  rule  is  less  abnormal  than  the 
other  coats,  but  it  is  sometimes  grossly  affected.  In  early 
cases  it  is  thickened  and  very  cellular,  with  httle  foci  of  mono- 
nuclear ceUs  scattered  here  and  there.  In  older  examples 
it  is  distinctly  sclerosed,  and  the  new-formed  tissue  is  more 
or  less  degenerate.  Here,  too,  as  in  the  intima  and  the  media, 
elastic  hyperplasia  and  degeneration  may  be  distinct.     The 


THE  DISEASES  OF  THE  ARTERIES  43 

vasa  vasorum  often  show  gross  disease,  the  arteries  being 
affected  by  an  endarteritis  obhterans,  and  the  veins  may  show- 
thickening  of  their  coats. 

Patchy  Mesarteritis.* — ^The  naked-eye  appearance  of  this 
form  resembles  in  some  degree  the  atheromatous  lesions.  The 
patches  in  the  early  stage  are  elevated  and  soft,  and  have  a 


Fig.  26. — Syphilitic  Mesaoetitis.     (x  150.) 

The  vasa  in  the  adventitia  show  endarteritis  obliterans,  and  are  surrounded  by 
many  mononuclear  cells. 

greyish  gelatinous  appearance,  and  are  generall}^  most 
numerous  in  the  first  (ascending)  part  of  the  aorta.  In  older 
cases  they  are  tough  and  fibrous  and  pearh^  white,  and  may 
present  a  depressed,  stellate-shaped  scar  (Fig.  11).  Calcareous 
deposits  are  infrequent,  and  are  never  massive,  and  ulceration 
does  not  occur. 

*  The  description  of  these  lesions  is  based  upon  the  syphilitic  form. 


44  DISEASES  OF  THE  HEART 

The  microscopic  picture  is  characteristic.  In  Ihe  early 
stage  the  vasa  in  the  adventitia  are  surrounded  b}-  clumps  of 
mononuclear  cells,  and  their  walls  are  infiltrated  and  thickened, 
and  their  lumen  is  narrowed  (Fig.  26).  The  media  shows  areas 
of  necrosis  (Fig.  27),  into  which  new-formed  branches  of  the 
vasa  penetrate,  surrounded  by  a  Yerj  cellular  granulation 
tissue;  and  the  intima  is  thickened  and  cellular  opposite  the 


Fig.  27. — Syphilitic  Mesaortitis,  showing  a  Patch  of  Necrosis  ix  the 

Media.     (x90.) 

patch.  In  older  specimens  the  adventitia  is  thickened  and 
sclerosed,  and  the  vasa  maj^  be  almost  completely  obstructed; 
the  media  may  have  disappeared  complete^  in  places  and 
be  replaced  by  new-formed  connective  tissue  (Fig.  29),  and 
the  intima,  invaded  by  the  vasal  branches,  though  thickened  to 
a  greater  or  a  less  degree,  may  show  some  cicatricial  slu-inking. 

Endarteritis     Obliterans.  —  Endarteritis    obliterans    occurs 
chiefly  in  the  smallest  arteries  and  the  arterioles;  it  is  often 


Fig,  28. — Syphilitic  Mesaortitis  (Elastic  Stain),  showing  the  Degenera- 
tion OP  THE  Elastic  Tissue  in  a  Gkantjlomatous  Patch.     ( x  90.) 


Fig.  29. — Syphtlitio  Mesaortitis  (Elastic  Stain),    (x  8.) 
The  media  (the  thick  black  iJne)  is  completely  destroyed  in  two  places. 


46 


DISEASES  OF  THE  HEART 


present  in  the  cerebral  arteries  and  in  the  vasa  of  the  aorta 
It  is  always  local  in  its  distribution,  and  never  involves  more, 
than  a  short  length  of  a  vessel,  but  as  the  whole  circumference 
of  the  wall  is  involved,  the  lumen  is  always  narrowed  and 
sometimes  completely  blocked,  and  its  clinical  importance  is, 
in  consequence,  considerable. 

The  intima  is  always  greatly  thickened,  the  new-formed  con- 
nective tissue  being  in  the  early  stage  loose  and  very  cellular, 


Fig.  30. — Endarteritis  OsLiTEEAisrs.     (  x  150.) 
(From  a  case  of  acute  rheumatism.) 


with  much  hypertrophy  of  the  elastic  elements,  (Fig.  30), 
but  in  the  later  stages  poorly  nucleated  and  hyahne,  with 
degeneration  of  the  new-formed  elastic  fibres.  The  tnedia 
may  be  but  little  altered  or  definitely  atrophied.  The  adven- 
titia  is  always  thickened,  sometimes  to  an  extraordinary  degree 
(Fig.  31),  and,  like  the  intima,  shows  new  formation  of  elastic 
tissue.     The  relative  thickness  of  the  intima  and  the  adven- 


THE  DISEASES  OF  THE  ARTERIES  47 

titia  varies  considerably  in  different  cases,  and  sometimes  one, 
sometimes  the  other,  shows  the  greater  change.  Gross  fatty 
or  calcareous  degeneration  is  rarely  met  with. 

Medial  Calcification. — ^Medial  calcification  occurs  in  two 
forms.  In  those  cases  of  atheroma  in  which  extensive  calci- 
fication of  the  thickened  intima  has  occurred,  the  medial  layers 
in  the  immediate  vicinity  may  be  similarly  affected.     It  also 


Fig.  31. — Syphilitic  Endaeteeitis  Obliterak-s.     (x  90.)     (A.  W.  H.) 
The  adventitia  is  greatly  hypertrophied. 

occurs,  however,  in  a  widespread  manner,  though  stiU  patchy 
in  distribution,  mthout  any,  or  with  only  minimal,  alterations 
in  the  intima.  In  this  case  it  is  most  often  found  in  the 
peripheral  arteries,  and  is  readily  detected  during  life  by  the 
finger,  which,  as  it  runs  along  the  vessel,  meets  now  a  hard 
and  now  a  soft  patch  (Fig.  32).  The  vessels  are  frequently 
dilated.  On  microscopic  examination  in  well-marked  cases 
the  proper  structure  of  the  media  has  wholly  disappeared,  and 


48 


DISEASES  OF  THE  HEART 


is  replaced  by  a  mass  of  calcareous  granules,  often  welded 
together  and  encircling  the  vessel.  In  the  larger  vessels  the 
whole  of  the  circumference  is  rarely  affected. 

The  Etiology  of  Focal  Lesions. — Local  lesions  own  a  local  cause, 
but  it  must  be  admitted  that  our  information  as  to  the  precise 

etiology  of  focal  ar- 
terial disease  is  at  pre- 
sent imperfect.  The 
distinction  between 
atheroma  and  patchy 
mesarteritis  is  impor- 
tant. In  the  former 
the  primary  lesion  is 
intimal  hyperplasia, 
and  the  media  atro- 
phies before  the  pres- 
sure of  the  nodule 
under  the  influence 
of  the  intra-arterial 
blood  -  pressure.  In 
the  latter  the  primary 
lesion  is  in  the  middle 
coat.  Patchy  mesar- 
teritis is  most  fre- 
quently due  to 
syphihs,  and  repre- 
sents the  reaction  pro- 
duced by  the  invasion 
of  spirochsetes  (which 
have  been  demon- 
strated in  situ  by 
Schmorl,  Burda, 
Wright,  and  Klotz),  or  follows  obstruction  of  the  vasa  in  the 
adventitia  and  resultant  medial  necrosis.  But  while  early 
lesions  may  be  accuratel}'  classified,  the  ultimate  scars  are 
essentially  similar,  and  the  question  must  be  approached  in  a 
general  way. 

Evidence  is  steadily  accumulating  in  favour  of  the  view 
that  the  infections  as  a  w^hole  are  a  not  uncommon  cause  cf 


Fig.  32. — Medial  Calcification-.     (J.  E.  R.) 
Skiagram  showing  the  ulnar  and  radial  arteries. 


THE  DISEASES  OF  THE  ARTERIES  49 

focal  lesions.  It  has  been  known  for  long  that  in  cases  of 
pysemia  patches  similar  in  their  nature  to  those  sometimes 
found  on  the  valves  of  the  heart  may  be  present  on  the  arterial 
walls,  and  that  an  infective  arteritis  may  occur  by  extension 
from  a  neighbouring  infective  focus  (Fig.  129).  As  a  rule, 
however,  bacteria  are  not  found  in  early  specimens  of 
atheroma,  and  spirochaetes  also  are  usually  absent  in  cases  of 
syphihtic  disease,  but  tubercle  baciUi,  pneumococci,  anthrax 
baciUi,  streptococci,  and  staphjdococci  have  all  been  found  in 
exceptional  cases.  Usually  the  infection  takes  place  from  the 
blood-stream,  but  an  embolic  origin  is  conceivable,  and  an 
acute  mesarteritis  has  been  observed  in  acute  rheumatism, 
enteric  fever,  and  diphtheria.  Plaques  of  recent  atheroma 
are  often  present  in  the  aortas  of  individuals  who  have  died 
from  acute  disease.  They  have  been  reported  in  cases  of 
smallpox,  diphtheria,  erj'sipelas,  pneumonia,  acute  rheumatism, 
influenza,  scarlatina,  measles,  and  enteric  fever,  being  present 
in  the  latter  in  twenty-one  of  fifty-two  'post-mortems  (Thayer 
and  Brush).  Experimental  research,  too,  has  shown  similar 
results,  and  intimal  changes  have  been  produced  by  inocula- 
tions with  streptococci,  medial  changes  with  diphtheria  toxin 
and  the  Micrococcus  rheumaticus,  and  intimal  and  medial 
■changes  in  conjunction  with  staphylococci. 

Josue's  experiments  with  adrenalin  have  opened  out  a  new 
field  of  observation.  He  showed  that  repeated  injections 
of  this  drug  into  rabbits  produced  local  thinning  and  calcifica- 
tion of  the  aortic  media  with,  in  some  cases,  a  local  thickening 
•of  the  overlying  intima;  and  his  results  have  been  confirmed 
by  numerous  observers.  Other  drugs,  too,  of  similar  h\-per- 
tonica  ction  (nicotine,  digitahn,  hydrastine,  barium  chloride) 
have  also  been  shown  to  produce  similar  results,  and  Croftan 
'has  produced  various  lesions  in  the  vessels  with  solutions 
of  xanthin  and  hj-poxanthin. 

The  exact  mechanism  of  these  procedures  is  not  3'et  under- 
stood, but  Klotz  has  sho^vn  that  medial  calcification  may 
follow  an  increase  of  the  blood-pressure  produced  by  suspending 
rabbits  by  the  hind-legs  for  short  periods  over  mam-  daj^s, 
the  lesions  being  confined  to  those  vessels  (carotids  and  aorta) 
in  which  the  blood-pressure  was  raised,  and  absent  in  those 


50  DISEASES  OF  THE  HEART 

below  the  diaphragm ;  atheromatous  lesions,  too,  were 
found  in  the  carotid  arteries,  which  suggests  that  both  medial 
and  intimal  lesions  maj-  result  from  elevation  of  the  blood- 
pressure. 

Although  it  is  not  difficult  to  demonstrate  the  various  ways 
in  which  focal  lesions  may  be  produced,  it  is  not  easy  to  define 
their  actual  causes,  taking  into  consideration  their  frequency 
in  persons  over  middle  age  and  their  special  sites  of  election 
in  the  arterial  tree. 

The  frequency  with  which  the}^  occur  makes  it  evident  that 
some  of  the  possible  causes  which  we  have  considered  have 
but  little  to  do  with  their  origin.  Tuberculosis  and  syphilis, 
for  example,  must  be  ruled  out  of  court,  for  these  diseases, 
though  prevalent  enough,  are  by  no  means  universal.  The 
infections  as  a  Avhole  can  hardly  be  responsible  for  many  cases . 
It  is  true  that  acute  arterial  lesions  are  not  infrequently  met 
^^dth  in  these  diseases,  but  post-mortein  records  show  that  gross- 
changes  are,  on  the  whole,  uncommon,  and  that  when  present 
they  are  rarely  extensive.  The  frequency,  however,  with 
which  infections  occur  during  life,  the  exanthemata  in  child- 
hood, and  influenza,  pneumonia,  enteric  fever,  etc.,  in  later 
years  make  it  possible  that  their  influence  is  greater  than  has 
been  otherwise  supposed,  and  that  the  little  lesions  thus 
initiated  may,  perhaps,  as  places  of  lessened  resistance,  allow 
other  causes  to  produce  greater  results  than  would  otherwise 
be  possible. 

Nodular  lesions  are  not  uncommon  in  cases  of  diffuse 
arterio-sclerosis.  The  lumen  of  the  smaller  vessels  is  often 
narrowed,  and  the  fibrous  overgrowth  of  the  adventitia  some- 
times spreads  into  the  tissues  and  produces  little  islets  of 
fibrosis  in  the  viscera,  entanghng  and  destroying  the  adjacent 
cells.  Any  of  the  organs  may  be  affected,  but  the  heart  and 
the  kidneys  are  chiefly  involved.  It  seems  probable  that  in 
arterio-sclerosis  nodular  lesions  vnsuj  arise  in  the  larger 
vessels,  such  as  the  aorta,  from  a  similar  affection  of  their 
vasa . 

On  the  whole,  however,  the  explanations  seem  insufficient,, 
and  other  causes  must  come  into  action. 

The  special  distribution  of  the  focal  lesions  has  long  been 


THE  DISEASES  OF  THE  ARTERIES  51 

held  to  indicate  that  mechanical  irritation  plays  an  important 
part  in  their  etiology.  The  buttressing  of  particular  parts 
of  the  arterial  system  shows  that  special  stress  obtains  at  these 
special  points  even  in  normal  circumstances ;  and  certain 
vessels,  such  as  the  corona.ry  arteries  of  the  heart,  the  intes- 
tinal arteries  and  those  of  the  limbs,  must  be  more  hable  to 
injury  than  those  contained  within  organs  which  move  but 
little  or  are  deeply  situated.  (Pophteal  aneurisms,  for  instance, 
seem  almost  to  have  disappeared  with  the  post-boys,  and 
tortuosity  of  the  temporal  arteries  is  of  common  occurrence, 
as  it  is  produced  by  the  pressure  of  the  hat  against  the  skull.) 
It  is  true  that  provision  seems  to  have  been  made  for  such 
varying  needs,  but  the  continued  slight  trauma  of  the  systolic 
pulse-waves  must  nevertheless  exert  an  influence  which  in 
time  will  produce  damage,  and  this  is  most  likely  to  occur  in 
cases  where  physical  labour  is  the  chief  occupation.  Medial 
calcification  is  thus  common  in  the  femoral  and  iliac  arteries 
of  persons  such  as  poHcemen,  who  are  constantly  standing, 
and  in  the  brachial  and  radial  arteries  of  individuals  whose 
work  entails  continued  use  of  their  arms,  and  is  even,  according 
to  Klotz,  more  common  on  the  right  side  in  right-handed 
persons.  The  arterial  blood-pressure  is  Mable  to  many  altera- 
tions from  phj^siological  influences,  and  these  are  almost 
always  in  the  direction  of  temporary  elevation  above  the 
normal.  Exercise,  the  ingestion  of  food,  cerebral  excitement, 
etc.,  all  produce  an  increase,  and  this  may  be  considerable 
if  the  stimulus  is  great  or  frequently  repeated,  and  the  proba- 
bihty  of  injurious  irritation  will,  under  these  circumstances, 
be  greater  than  in  normal  conditions. 

The  form  and  site  of  the  initial  lesion  depend  upon  several 
factors.  In  some  instances  overuse  of  limbs  leads  to  their 
special  involvement;  in  other  cases  the  aortic  strain  may  be 
greatest;  in  others,  again,  a  previous  lesion  may  suggest  a 
particular  site. 

The  special  HabiHty  of  the  aorta  and  the  cerebral  arteries 
to  syphilitic  disease  has  not  yet  obtained  a  satisfactory  ex- 
planation, but  it  maj'  be  pointed  out  that  their  structure  is 
very  speciahzed,  and  that  the  aorta  is  exposed  to  the  full 
force  of  the  ventricular  systole,  while  disease  of  the  cerebral 
arteries  is  so  prejudicial  to  the  proper  working  of  the  brain. 


52  DISEASES  OF  THE  HEART 

and  even  to  life  itself,  that  it  has  probably  attracted  more 
than  its  fair  share  of  attention. 

Endarteritis  obhterans  is  not  always  of  pathological  sig- 
nificance. It  occurs,  for  instance,  in  the  umbiHcal  vessels  after 
their  special  function  has  ceased ;  in  the  ^vessels  of  a  stump 
after  amputation;  and  in  arteries  whose  lumen  has  been 
narrowed  or  obstructed  by  any  cause,  the  normal  proliferative 
changes  exceeding  the  degree  which  is  required. 

It  is  of  common  occurrence  in  the  infections,  and  has 
been  found  in  acute  rheumatism,  diphtheria,  scarlatina, 
smallpox,  and  enteric  fever.  It  is  particularly  frequent  in 
tuberculosis  of  the  cerebral  membranes  and  in  syphilis,  the 
adventitial  changes  in  the  latter  case  being  usually  extreme. 

Medial  calcification  is  most  frequently  associated  with 
mechanical  sources  of  irritation. 

1.  Arterio-Sclerosis. — A  diffuse  affection  involving  the  whole 

arterial  tree. 

Caused  by  High  Blood-Pressure: 

{a)  Associated  with  renal  disease. 

(6)  From  "repletion,"  relative  or  absolute. 

(c)  From  intoxications  due  to — 

(1)  Metabolic  errors;  gout,  digestive  disturb- 

ances, etc. 

(2)  Poisons    introduced    from    without — lead, 

nicotine,  etc. 

(d)  Following  the  infections. 

(e)  In  polycythsemia. 

2.  Focal  Lesions. — A  patchy  affection  involving  small  por- 

tions of  the  arteries. 
{a)  Infective  Lesions:  due  to  staphylococci,  strepto- 
cocci,   B.    anthrax,    B.    tuberculosis,    Spirochceta 
pallida. 
(6)  Without  Definite  Evidence  of  Infection: 
(1)  Atheroma,  caused  by — 

(i.)  The  infections:  Enteric  fever,  tuber- 
culosis, diphthjeria,  smallpox, 
measles,  scarlatina,  erysipelas,  pneu- 
monia, acute  rheumatism,  influenza. 


THE  DISEASES  OF  THE  ARTERIES  53 

(ii.)  Intermittent  elevation  of  the  blood- 
pressure. 

(2)  Mesarteritis,  caused  by — 

Syphilis,  acute  rheumatism,  enteric  fever, 
diphtheria . 

(3)  Endarteritis  obliterans,  caused  by — 

(i.)  Syphilis,  tuberculosis,  acute  rheu- 
matism, diphtheria,  scarlatina, 
smallpox,  enteric  fever. 

(ii.)  Occlusion  of  the  lumen  from  whatever 
cause. 

(4)  Medial  Calcification,  caused  by — 

(i.)  Trauma  (excessive  use  of  limbs,  inter- 
mittent or  continuous  elevation  of 
the  blood-pressure), 
(ii.)  Adrenalin,  nicotine,  digitalin,  hydras- 
tine,  barium  chloride. 


REFERENCES. 
John  Cowan: 

A  Review  of  Recent  Work  upon  Blood-Pressure.     Practitioner,  1904, 

vol.  Ixxiii.,  p.  218. 
The  Current  Theories  regarding  the  Causation  of  Arterio-Sclerosls.  Ibia., 
1905,  vol.  Ixsv.,  p.  203;  ihid.,  1906,  vol.  Ixxvi.,  p.  317;  ihid.,  1909,  vol. 
Ixxxiii.,  p.  614;  ihid.,  1911,  vol.  Ixxxvi.,  p.  750. 
The  Influence  of  the  Acute  Infections  upon  the  Arteries.     Glasgow  Med. 
Joum.,  1906,  vol.  Ixvi.,  p.  88. 
Louis  Galiavaed in:  La  Tension  Arterielle  en  Clinique.     Paris,  1910. 
H.  Hitohakd:    Arterio-Sclerose.     Paris,  1910. 

T.  C.  Janeway:    The  Clinical  Study  of  Blood- Pressure.     New  York,  1904. 
O.  Josue:   Traite  de  I'Arterio-Sclerose.     Paris,  1909. 
O.  Klotz:   Arterio-Sclerosis.    Diseases  of  the  Media.    Publications  from  th  e 

University  of  Pittsburgh  Medical  School,  1911. 
W.  Russell:  Arterial  Hypertonus.    Edinburgh,  1907. 


CHAPTER  III 
THE  SYMPTOMS  OF  ARTERIAL  DISEASE 

The  symptoms  of  arterial  disease  vary  greatly  in  different 
patients,  as  they  depend  both  upon  the  variety  of  the  arterial 
lesion  and  upon  its  special  site,  and  are,  in  the  majority  of 
cases,  the  results  of  defective  function  of  the  various  viscera 
rather  than  an  indication  of  the  process  which  has  produced 
them.  The  symptoms  of  an  aneurism,  for  example,  arise 
chiefly  from  pressure  upon  neighbouring  structures,  and  tumour 
and  pulsation  are  the  only  evidence  of  the  arterial  dilatation. 

The  two  main  groups  of  arterial  disease  contrast  in  almost 
every  particular.  In  the  focal  or  nodular  group  the  lesions 
are  always  local  and  never  of  great  size,  although  they  may  be 
numerous,  and  by  coalescence  affect  considerable  tracts  of  the 
vessels.  The  larger  arteries  are  chiefly  involved.  In  atheroma 
and  mesarteritis  the  wall  is  weakened,  and  dilatation  of  the 
vessel,  or  even  rupture,  may  ensue.  In  medial  calcification 
the  artery  is  often  wider  than  normal.  In  endarteritis 
obhterans  the  arterial  lumen  is  narrowed,  and  thrombosis 
often  follows,  a  result  which  is  unusual  in  the  others. 

In  arteriosclerosis,  on  the  other  hand,  the  whole  of  the 
arterial  tree  is  involved,  and  the  change  is  most  considerable 
in  the  smaller  vessels.  The  walls  are  thickened  and  on  the 
whole  strengthened,  so  that  dilatation  or  rupture  is  uncommon 
fcT.ve  in  the  cerebral  arteries,  where  miliary  aneurisms,  the 
common  cause  of  cerebral  haemorrhage,  are  often  found. 
Thrombosis  is  comparatively  rare,  but  the  lumen  is  generally 
narrowed,  and  the  visceral  blood-supply  may  be  hmited  in 
consequence. 

The  focal  lesions  may  be  widespread,  and  even  extreme, 
without  causing  any  abnormal  strain  uponjthe  left  ventricle. 

54 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE  55 

In  other  cases,  however,  where  the  thoracic  aorta  or  the 
splanchnic  arteries  are  involved,  the  left  ventricle  may  be 
considerably  hypertrophied.  In  arterio-sclerosis,  on  the  other 
hand,  the  left  ventricle  is  always  hypertrophied,  sometimes  to 
an  extraordinary  degree;  and,  as  in  valvular  disease,  the 
reserve  power  is  necessarily  more  limited  than  in  health,  and 
the  "  field  of  response  "  is  correspondingly  diminished.  The 
essential  cause  of  arterio-sclerosis  is  continued  elevation  of  the 
arterial  pressure,  and  the  arteries  as  well  as  the  heart  are  at 
first  thickened  by  muscular  hjrpertrophy.  In  time,  however, 
fibrosis  supervenes,  and  their  elasticity  is  largely  lost. 

One  must  distinguish  between  the  two  types  of  arteries. 
One  set  are  the  "  mains  "  for  the  distribution  of  the  blood, 
affording  an  elastic  assistance  to  the  heart,  and  insuring  a  con- 
tinuous flow,  at  equable  pressures,  through  the  capillaries. 
The  other  set  are  the  "supply-pipes," with  "taps  "which can 
be  shut,  at  any  rate  partially,  and  thus  alter  the  distribution 
of  the  blood  among  the  various  organs  as  necessity  dictates. 
If  the  mains  are  rigid,  the  heart  has  more  work  to  do,  and  the 
capillary  current  is  less  even  in  its  flow.  If  the  supply-pipes 
are  stiff,  the  "  taps  "  cannot  be  altered  at  discretion,  and 
variations  in  the  functional  demands  of  the  tissues  can  only  be 
inadequately  supplied,  and  that  by  variations  in  the  general 
blood-pressure  and  an  increased  strain  upon  an  already  over- 
taxed ventricle. 

The  symptoms  in  the  two  groups  arise  in  different  ways. 
In  the  focal  cases  they  are  the  results  of  hcemoirhage,  thrombosis, 
or  arterial  dilatation.  The  results  of  haemorrhage  vary  mainly 
■with  its  amount,  and  also,  to  some  extent,  with  its  site,  cere- 
bral haemorrhage,  for  instance,  causing  death  with  a  loss  of 
blood  which,  if  external,  would  occasion  little,  if  any,  discom- 
fort. The  results  of  thrombosis  depend  both  upon  its  site 
and  upon  the  rapidity  of  the  closure;  sudden  occlusion  of  a 
coronary  artery  may  produce  myocardial  infarct  or  rupture 
of  the  heart,  while  a  gradual  narrowing  may  allow  of  com- 
pensatory dilatation  of  anastomotic  vessels,  with  but  little 
interference  with  the  nutrition  of  the  cells  involved.  The 
results  of  dilatation  depend  mainly  upon  its  extent  and  its 
site,  and  are  most  marked  when  it  obtains  within  a  cavit}-  of 


56  DISEASES  OF  THE  HEART 

fixed  dimensions- — e.g.,  within  the  cranium  or  the  thorax. 
The  lesions  which  are  thus  produced  are  as  a  rule  isolated  and 
single,  though  sometimes  of  considerable  size. 

In  arteriosclerosis  visceral  lesions  are  widespread,  multiple, 
and  individually  of  trifling  degree,  though  their  collective  in- 
fluence may  be  great.  Dilatation  and  haemorrhage  are  un- 
usual, save  in  the  case  of  the  cerebral  arteries,  and  thrombosis 
is  also  infrequent.  But  the  lumen  of  the  vessels  is  often 
narrowed,  and  the  visceral  blood-supply  is  in  consequence 
diminished — an  effect  which  is  intensified  by  the  limitation  of 
the  response  to  vasomotor  influences  entailed  by  the  fibrosis 
of  the  vessel  walls.  This  fibrosis,  too,  not  infrequently  spreads 
into  the  tissues  from  the  adventitia,  and  produces  little  islets 
of  fibrosis  in  the  organs,  entangling  and  destroying  the  ad- 
jacent cells.  Any  of  the  viscera  may  be  involved,  but  the 
heart  and  the  kidneys  are  the  common  sufferers .  Renal  changes 
are  the  rule  in  arterio-sclercsis.  The  initial  fault  is  often 
renal,  a  cirrhosis  of  acute  or  chronic  type;  and  a  somewhat 
similar  condition,  the  arterio-sclerotic  kidney,  is  generally  more 
or  less  evident  in  cases  which  have  arisen  from  other  than  renal 
fault. 

The  symptoms  of  the  two  groups  contrast  correspondingly. 
In  the  focal  group  aneurism,  infarct,  and  haemorrhage  are 
the  essential  conditions.  In  arteriosclerosis  the  heart  is 
always  overtaxed,  renal  excretion  is  generally  inadequate,  and 
other  viscera  are  apt  to  be  damaged ;  while  their  function  is  still 
further  impaired  by  the  limitation  of  their  blood-supply  pro- 
duced by  the  arterial  disease  and  the  relative  cardiac  insuffi- 
ciency. At  first  symptoms  only  occur  on  special  strain, 
whether  physical,  mental,  or  visceral ;  but  ultimately  even  the 
normal  work  is  imperfectly  performed.  The  onset  of  symptoms 
is  thus  insidious,  unless  some  special  cause  precipitates  their 
advent.  In  the  focal  group  symptoms  often  ensue  suddenl}^, 
and  are  acute  from  the  outset. 

"^  From  yet  another  standpoint  the  two  groups  contrast.  The 
causes  of  the  first  group  are  numerous,  syphihs,  tuberculosis, 
trauma,  intoxications,  and  infections  of  various  kinds;  and 
while  some  of  these  may  be  continuous  in  their  action,  others 
have  only  a  hmited  period  of  harmful  activity.     Focal  lesions 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE         57 

may  thus  be  progressive  or  merely  the  healed  scars  of  ancient 
wounds.  Arterio-sclerosis,  on  the  other  hand,  is  due  to  con- 
tinued high  arterial  pressure;  and  although  in  some  cases  the 
initial  elevation  is  probably  of  functional  origin,  and  so  re- 
movable on  removal  of  its  cause,  in  others  it  is  secondary  to 
visceral  lesions  which  are  incurable.  When  once  permanent 
changes  have  occurred  in  the  vessels,  the  high  pressure  is  per- 
manent ;  the  strain  upon  the  heart  and  vessels  continues ;  and, 
as  time  goes  on,  the  lesions  inevitably  progress. 

The  symptoms  in  arterial  disease  may  thus  be  produced  in 
various  ways,  and  as  they  may  be  related  to  almost  any  organ, 
and  may  simulate  even  closely  symptoms  due  to  other  patho- 
logical lesions,  their  exact  significance  may  be  difficult  to 
determine.  This  is  particularly  the  case  with  the  focal 
diseases.  In  arterio-sclerosis  the  under Ijdng  general  condi- 
tion can  in  most  cases  be  readily  recognized. 

The  essential  and  constant  feature  in  arterio-sclerosis,  at 
any  rate  until  cardiac  failure  is  weU  marked,  is  elevation  of  the 
aortic  blood-pressure.  In  a  large  group  of  cases,  renal  cir- 
rhosis occurs,  if  not  antecedent  to,  at  least  pari  passu  with,  the 
cardio-vascular  changes  which  are  compensatory  and  per- 
manent. Sometimes  the  cardio-vascular  hjrpertrophy  is  not 
well  marked,  and  death  then  seems  to  ensue  more  rapidly  than 
is  the  rule  when  the  hypertrophy  is  considerable.  The  cause  of 
the  failure  may  he  in  anaemia  and  debihty  consequent  on  the 
renal  disease  or  other  coincident  causes,  but  is  sometimes,  at 
any  rate,  congenital  in  origin.  We  cannot  all  of  us  become 
Sanclows,  even  if  we  follow  a  similar  hne  of  training,  and  the 
vascular  musculature  is  in  many  w^ays  comparable  to  the 
muscles  of  the  hmbs. 

But  in  another  group  of  cases,  as  Sir  Chfford  Allbutt  has 
urged,  no  renal  disease  at  first  coexists.  The  primary  fault  is 
an  intoxication  of  varied  origin,  w^hich  produces  an  increase 
of  the  peripheral  resistance,  and  consequent  elevation  of  the 
aortic  blood-pressure;  but  an  elevation  which  at  first  depends 
upon  removable  causes,  and  can  thus  for  a  time  be  dissipated 
by  suitable  treatment.  "^ 

The  recent  introduction  into  clinical  methods  of  the  Riva- 


58 


DISEASES  OF  THE  HEART 


Rocci  sphygmomanometer  and  its  numerous  modifications  has 
put  within  the  reach  of  the  practitioner  a  method  by  which  the 
arterial  pressure  may  be  measured  with  fair  accuracy,  and 
without  any  special  difficulty  of  technique.     But  while  it  is 


12Q, 

7' 


■  -VlAU  ^AA^AVMUJ\f^MM/J^'^~VJ 


VlWMAMMWWMMl 


Aortic 


Fig.  33. — Blood-Pkessure  Tracing  (Gibson  Sphygmomanometer) 

Regurgitation. 

The  pulse  is  much  larger  than  in  Fig.  34,  though  the  systolic  blood-pressure  is 
much  lower.     The  pulse-pressures  are  equal. 

useful  to  have  figures  which  can  be  contrasted,  and  give  a 
measure  in  some  way  of  the  severity  of  the  disturbance,  it 
must  be  remembered  that  the  blood-pressure  varies  to  a  con- 
siderable extent  in  the  healthy  individual  from  causes  of  a 
temporary  and  often  trivial  nature  (emotion,  exercise,  diet, 


THE  SY^IPTOMS  OF  ARTERIAL  DISEASE 


59 


■NW^ 


Fig.  34.— Blood-Pressuee  Tracing  (Gibson  Sphygmomanometek): 
Chronic  Nephritis, 

Contrast    with  Fig.    33. 

etc.),  the  influence  of  which  cannot  always  be  accurately 
correlated,  and  that  similar  results  may  be  noted  even  in  well- 
marked  examples  of  high  blood-pressure.  The  earlier  readings  m 


60  DISEASES  OF  THE  HEART 

hospital  patients  confined  to  bed  are  often  shown  by  continued 
observation  to  be  inaccurate,  from  causes  of  this  temporary 
kind,  and  but  little  importance  should  be  attached  to  isolated 
observations,  though  daily  records  are  of  considerable  value. 

The  information  which  is  desired  can,  too,  be  obtained  from 
other  data.  Digital  examination  of  the  pulse  is  at  the  present 
day  too  much  depreciated ;  and  while  I  must  acknowledge  that 
my  impressions  of  the  arterial  pressure  from,  such  exam.inations 
have  not  infrequently  been  at  variance  with  instrumental 
readings,  a  constant  comparison  has  led  to  greater  accuracy. 
The  error  seems  to  Me  in  the  failure  to  appreciate  that  the 
size  of  the  pulse-wave  and  the  amount  of  the  pulse-pressure* 
have  no  constant  relation  to  the  height  of  the  aortic  pressure; 
to  take  a  concrete  example,  the  large  quick  pulse  of  aortic 
regurgitation  may  be  of  much  lower  pressure  than  a  small 
but  wir}-  pulse  (Figs.  33,  34). 

The  sphj'gmomanometer,  too,  gives  no  information  with 
regard  to  the  condition  of  the  arterial  walls,  information  which 
is  readily  afforded  by  the  finger;  and  if  all  the  accessible 
arteries  (retinal,  radial,  brachial,  temporal,  facial,  femoral, 
dorsahs  pedis)  are  explored,  a  fairlj'  accurate  idea  of  the  con- 
dition of  the  vessels  as  a  whole  may  be  obtained.  It  is  true 
that  the  condition  of  the  peripheral  and  the  visceral  vessels 
by  no  means  always  corresponds,  and  changes  may  be  extreme 
in  one  set  without  the  other  being  seriousty  involved,  but  on 
the  whole  the  comparison  is  apt .  The  failure  in  correspondence 
is  seen  chiefly  in  the  focal  lesions ;  in  arterio -sclerosis  the  asso- 
ciation is  more  absolute,  so  that,  while  irregularities  in  the 
vessel  walls  convey  only  a  hmited  significance,  general  thicken- 
ing is  always  important.  The  ophthalmoscopic  evidence  may 
be  unmistakable. 

Examination  of  the  heart  is,  of  course,  equally  essential. 
A  weU-sustained  apex  impulse  displaced  downwards  into  the 
sixth  or  seventh  interspace,  prolongation  and  cluUing  of  the 
first  apical  sound,  and  accentuation  of  the  second  aortic  sound 
are,  in  the  absence  of  valvular  flaws,  positive  evidence  of  high 
aortic  blood-pressure.     The  second  aortic  sound  may  be  in- 

*  The  pulse-pressure  is  the  difierence  in  pressure  between  the  systolic  and 
the  diastolic  pressures. 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE 


61 


toned  and  ringing  in  quality,  but  this  is  probably  due  to  aortic 
dilatation,  whether  local  or  diffuse. 

It  is  easy  to  recognize  such  cases  when  they  come  under 
observation  from  casual  reasons,  such  as  insurance  examination, 
etc.,  at  a  time  when  the  compensatory  mechanism  is  well 
estabhshed  and  sufficient,  and  symptoms  are  in  abeyance,  but 
an  accurate  diagnosis  may  be  extremely  difficult  in  the  later 
stages  if  cardiac  failure  has  supervened.  The  blood-pressure 
may  be  within  normal  limits,  the  second  aortic  sound  may  not 
be  notably  emphatic,  and  the  first  apical  sound  may  be  short 
and  sharp,  or  obscured  by  murmur  if  the  mitral  valve  has 
given  way  before  the  strain. 

Cardiac  hypertrophy  is  not  necessarily  associated  with  high 
arterial  pressure.  In  well-compensated  cases  of  mitral  regur- 
gitation and  aortic  stenosis,  for  example,  the  degree  of  ven- 
tricular hypertrophy  is  simply  that  required  to  insure  the 


Fig.  35.— Pulse  of  Aortic  Regurgitation. 


entrance  into  the  aorta,  in  the  proper  time,  of  the  proper 
amount  of  blood  at  the  proper  pressure.  In  aortic  regurgita- 
tion other  factors  come  into  operation.  If  an  average  amount 
of  blood  is  to  be  left  in  the  arteries  at  the  end  of  diastole,  the 
amount  which  is  thrown  into  them  during  systole  must  be 
greater  than  normal,  so  as  to  allow  for  that  which  returns  into 
the  ventricle  as  soon  as  systole  has  ceased ;  and  the  rapid  fall 
of  pressure  during  diastole  requires  an  excessive  systolic 
pressure.  The  pulse-pressure  is  the  true  index  of  the  degree 
of  the  mechanical  fault.  But  such  a  pulse  differs  notably  from 
that  associated  with  granular  kidneys ,  In  aortic  regurgitation, 
as  sphygmographic  tracings  show  so  well  (Eig.  35),  the  pressure 
faUs  rapidly,  and  the  mean  pressure  is  low  relatively  to  the 
maximum.  In  renal  cases  the  pressure  is  well  maintained, 
and  the  mean  pressure  is  high  relatively  to  the  maximum. 
A  high  blood-pressure  is  not  invariably  evidence  of  cardiac 


62 


DISEASES  OF  THE  HEART 


sufficiency,  and  may,  indeed,  be  accompanied  by  definite  signs 
of  cardiac  failure.  The  most  striking  example  which  I  have 
observed  occurred  in  a  man,  aged  fifty-one,  who  was  com- 
plaining of  breathlessness  and  slight  oedema  of  the  feet.  The 
sudden  occurrence  of  a  left  facial  pals}^,  accompanied  by  some 
difficult}^  in  speech,  followed  a  few  days  later  by  a  partial 
right  hemiplegia,  was  considered  to  be  the  result  of  cerebral 
haemorrhage,  as  the  systohc  brachial  pressure  varied  from 
170  to  210  mm.  Hg.     But   'post-mortem  examination  revealed 


DEC. 

Hg. 
mm. 

200 
190 
180 
170 
160 
150 
140 
130 
120 
no 
100 
90 
80 
70 


12 

14 

W 

18 

21 

23 

25 

27 

30 

\ 

\ 

\ 

\ 

\ 

•^ 

--^ 

\ 

\ 

N. 

V 

N 

\ 

^ 

^^ 

\ 

\ 

\ 

V. 

Fig.  36. — Blood-Pressure  Chart. 

M.,  aged  47:  Chronic  nephritis,  bronchitis; 
steady  improvement. 


2 

12 

26 

Steady 
Progress 

/ 

J 

f 

/ 

E 

/ 

.g^ 

^ 

^ 

k 

fEB 

Hg. 
mm. 

170 

IGO 

150 

140 

130 

120 

no 

100 

90 

80 

70 

Fig.  37.— Blood-Pres- 
sure Chart, 

M.,  aged  57:  Aortic  val- 
vular disease;  steady 
improvement. 


in  the  cortical  vessels  multiple  emboli  which  were  derived  from 
clots  in  the  dilated  left  ventricle.  And  the  highest  pressure 
which  I  have  observed — 270  mm.  Hg — occurred  in  a  man 
who  became  breathless  on  the  least  exertion,  and  developed 
oedema  in  the  feet  and  legs  whenever  he  v/as  allowed  out  of 
bed. 

Such  failure  is,  of  course,  relative  and  not  absolute.  The 
ventricular  waU  may  be  greatly  thickened,  and  the  cells  may 
be  normal  on  microscopic  examination,  but  the  heart  may  yet 
be  overtaxed  and  unable  to  accomphsh  its  necessary  work. 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE 


63 


Cardiac  strain  may  arise  in  two  different  ways.  The  heart 
may  be  unable  to  overtake  extra  work  imposed  upon  it,  or 
may  from  intrinsic  causes  (fibroid,  fatty  degeneration,  etc.) 
be  unable  to  accomplish  even  a  normal  amount.  The  arterial 
pressure  may  thus  vary  either  upwards  or  downwards  in  the 
presence  of  symptoms,  and  it  may  be  impossible  for  a  time 
to  say  whether  the  actual  pressure  is  too  high  or  too  low  for 
the  particular  individual.  If  improvement  occurs,  the 
pressure  may  rise  or  fall;  as  death  approaches,  it  may  also 
rise  or  fall.     In  Fig.  36  the  pressure  is  seen  to  faU  coincidently 


APRIL    1908        MAY  JUNE 


23 

24 

25 

26 

/ 

r 

^ 

/ 

y 

V 

y 

^ 

NOV 

Hg. 
mm. 

170 
160 
150 
140 
130 
120 
110 
100 

90 

80 

70 

Fig.  38.— Blood. 

Presstjre  Chart. 

M.,  aged  40  :  Alcohol- 
ism ;  pneumonia. 
Death  on  Novem- 
ber 26. 


Hg. 
mm. 

170 
160 
150 
KO 
130 
120 
110 
100 
90 
80 
70 

F., 


J7 

25 

29 

7 

29 

8 

13 

17 

28 

3 

8 

\ 

V 

\ 

A 

V 

\ 

\ 

\ 

*v. 

V 

"-v^ 

^^ 

^ 

\ 

\ 

\ 

\^ 

^\ 

< 

_a^ 

^^ 

— 

V 

.'•^ 

Fig.  39. — Blood-Pressure  Chart. 
aged  35  :  Mitral  disease.     Death  on  July  23. 


with  improvement  in  the  general  condition;  in  Fig.  37  the 
pressure  rose  with  improvement;  in  Fig.  38  the  pressure  rose 
as  death  approached;  in  Fig.  39  it  fell. 

The  blood-pressure  may  be  elevated  for  a  time  independently 
of  arterial  or  renal  disease.  Fig.  40  shows  the  blood-pressure 
in  a  man,  aged  thirty-eight,  who  was  an  iron-moulder  by  trade. 
He  had  always  been  healthy,  save  for  an  attack  of  pneumonia 
at  the  age  of  twenty-three,  but  had  caught  cold  a  fortnight 
before  admission,  though  this  had  not  kept  him  away  from 


64 


DISEASES  OF  THE  HEART 


MARCH   WOS 


work.  Ten  days  later  he  noticed  that  his  eyelids  were  swollen 
in  the  morning,  but  the  swelling  disappeared  as  the  day  wore 
on;  his  back,  he  said,  was  sore  when  he  stooped.  He  had  a 
headache  next  day,  and  his  feet  were  swollen  at  night.  On 
admission,  all  these  symptoms  had  lessened.  There  was  a 
trifling  albuminuria,  and  a  little  oedema  in  the  legs  below  the 
knees,  but  the  latter  soon  disappeared.  The  urinary  output 
was  always  ample,  and  the  albuminuria  was  trifling,  and  some- 
times absent.     But  it  was  eight  days  before  the  pressure  fell 

within  normal  limits, 
and  three  weeks  more 
before  the  minimum 
reading  was  recorded. 
There  was  no  evidence 
otherwise  of  organic 
disease,  and  the  eleva- 
tion of  blood-pressure 
was  presumably  toxic 
in  origin. 

High  blood  -  pres- 
sure per  se  is  thus  no 
certain  evidence  of 
arterio-sclerosis,  as  it 
may  be  due  to  tem- 
porary causes,  and 
obtains  in  some  forms 
of  valvular  disease  of 
the  heart.  In  the 
absence  of  aortic  re- 
gurgitation, however, 
its  indefijiite  persistence  despite  treatment,  and  the  presence 
of  hypertrophy  of  the  left  ventricle,  are  extremely  suggestive 
of  the  disease.  Widespread  focal  lesions  in  the  thoracic  aorta 
or  the  splanchnic  arteries  are  the  only  other  factors  which  can 
produce  such  a  condition. 

The  apex  impulse  is  an  uncertain  guide  in  some  cases  of 
arterio-sclerosis.  It  may  be  hidden  by  pulmonary  emphysema, 
which  not  infrequently  ensues  in  arterio-sclerotic  cases.  It 
may  be  weak,  diffuse,  and  ill-sustained  if  cardiac  failure  has 


Hg. 
mm. 

210 
200 
190 
160 
170 
160 
150 
140 
130 
120 
no 
100 
90 
80 
70 


18 

20 

22 

25 

26 

30 

31 

8 

16 

19 

23 

— ♦— 

\ 

> 

V 

\ 

\ 

L 

A 

V 

\ 

\ 

K 

Ni 

^S 

N^ 

?«*s; 

^^ 

•v 

5s*-. 

\ 

V 

A 

V 

\ 

V 

. 

/^ 

^x 

^ 

Fig.  40. 


-Blood-Pkessube  Chakt. 
M.,  aged  38. 


THE  SYIVIPTOMS  OF  ARTERIAL  DISEASE         65 

supervened;  but,  on  the  other  hand,  may  still  be  punctate, 
powerful,  and  well  sustained  even  when  oedema  is  widespread 
and  general.  In  emphysema  the  cardiac  sounds  may  often  be 
heard  best  outside  the  left  border  of  the  cardiac  duhiess,  even 
in  the  axillary  line,  thus  indicating  enlargement  of  the  ventricle. 

The  cardiac  sounds  cannot  be  relied  upon.  The  second 
aortic  sound  may  be  weakened,  with  failure,  to  such  a  degree 
as  to  be  within  normal  limits,  though  it  is  often  distinctly 
emphatic ;  or  it  may  be  whoUy  obscured  by  murmur.  The 
special  qualities  of  the  first  apical  sound  are  often  at  fault,  and 
it  teUs  merely  of  mitral  reflux  or  myocardial  weakness. 

In  the  absence  of  these  data,  the  condition  of  the  arteries 
may  still  be  sufficient  evidence,  and  it  is  here  that  ophthalmo- 
scopic examination  is  so  valuable,  as  the  changes  are  present  in 
the  large  majority  of  cases,  and  persist  irrespective  of  cardiac 
insufficiency.  ^ 

The  presence  or  absence  of  albuminuria  is  of  little  value  from 
the  diagnostic  point  of  view.  Renal  disease  is  a  common 
accompaniment  of  arterio-sclerosis,  but  it  may  also  occur  in- 
dependently. The  small  red  kidney  and  the  arterio-sclerotic 
kidney  are  usually  associated  with  an  albuminuria  which  is 
trifling  in  degree,  and  may  even  be  wholly  absent,  at  any  rate 
for  a  time;  and  the  coincidence  of  considerable  albuminuria 
indicates  the  presence  of  some  new  factor,  such  as  passive 
venous  congestion  or  some  accidental  intoxication  or  toxaemia. 

The  symptoms  which  are  met  with  in  arterio-sclerosis  are 
quite  as  varied  as  one  would  expect  from  consideration  of  the 
pathological  lesions.  Few  of  the  viscera  are  absolutely  normal, 
and  any  one  of  them  may  be  specially  damaged.  But  the 
kidneys  are  almost  always  more  or  less  involved,  and  renal 
excretion  is  frequently  inadequate;  and  the  heart,  habitually 
working  close  to  its  maximum  power,  has  a  reserve  which  is 
but  small,  and  in  consequence  readily  exhausted;  so  that  in 
practice  cardiac  and  renal  symptoms  form  the  bulk  of  the  com- 
plaints. 

The  symptoms  which  ensue  on  cardiac  failure  do  not  differ 
appreciably  from  those  that  may  occur  in  cardiac  insufficiency 
due  to  other  causes ;  shortness  of  breath,  palpitation  or  other 
cardiac    discomforts,    gastro-intestinal    disturbances,    oedema, 

5 


66 


DISEASES  OF  THE  HEART 


etc.,  are  tlie  common  complaints.  In  the  earlier  stages,  when 
the  failm-e  is  slight  and  relative,  the  diagnosis  is  easily  made 
on  routine  examination;  but  in  the  later  stages,  and  in  Ihe 
presence  of  well-defined  valvular  flaws,  one  is  apt  to  miss  the 

underlying  general  condition. 
Valvular  flaws  may  arise 
in  various  ways.  Arterio- 
sclerosis may  hit  a  patient 
whose  heart  is  already 
damaged  by  an  acute  endo- 
carditis, or  the  converse  may 
obtain.  Arterio-sclerosis  may 
cause  local  lesions  in  the- 
arteries  as  well  as  in  the 
viscera,  and  the  valves  may 
be  deformed  by  a  chronic 
degenerative  lesion.  The 
ventricle  may  give  way  before 
the  strain,  and  dilate,  with 
relative  mitral  insufficiency. 
French  "v\Titers  are  in  the  habit 
of  emphasizing  this  difference 
in  origin  of  mitral  reflux  by 
the  statement  that  in  one 
group  the  lesion  begins  at  the 
valves  and  ends  at  the 
myocardium,  while  in  the 
other  it  begins  in  the  myocar- 
dium and  ends  at  the  valves. 
In  uncomphcated  cases  of 
mitral  disease  the  sequel  of 
rheumatic  endocarditis,  the 
blood-pressure  is  uniformly 
normal  or  below  normal.  It 
is  commonly  asserted  that 
the  presence  of  oedema  causes  variations  in  the  blood-pressure 
readings  from  the  pressm^e  exercised  upon  the  capillary  network 
in  the  tissues,  but  my  own  experience  is  not  consonant  with  this 
conclusion.   The  presence  of  oedema  in  the  arms,  however,  inter- 


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THE  SYMPTOMS  OF  ARTERIAL  DISEASE 


67 


JUNE  190R 


fering  with  the  proper  apposition  of  the  armlet  or  the  correct 
appreciation  of  the  radial  pulse,  of  necessity  introduces  factors 
which  areHkely  to  prevent  accurate  records ;  but  in  its  absence 
it  is  astonishing  to  find  how  little  variation  occurs  even  in  the 
presence  of  notable  s^-mptoms.  In  Fig.  41,  for  example,  the 
systohc  pressure  only  varied  from  120  to  95  mm.  Hg.  diu-ing 
the  course  of  observations  extending  over  nearly  six  months. 
The  patient,  who  was  aged  thirty,  was  admitted  mth  orthop- 
noea,  dropsy  invading  the  trunk,  ascites,  and  much  catarrh 
in  the  chest.  For  a  time  all 
these  symptoms  were  in  abey- 
ance, and  she  was  out  of  bed 
and  walking  about  the  ward 
\^dthout  discomfort,  but  the 
improvement  was  only  tem- 
porary. She  spat  blood  for 
over  a  month  from  pulmonary 
infarcts,  and  ultimate!}^  left 
hospital  during  a  reciurence 
of  the  symptoms .  The  highest 
readings  were  obtained  at  a 
time  when  compensation  was 
fairly  well  estabhshed. 

But  other  mitral  cases  occur 
with  symptoms  of  a  similar 
kind  in  which  the  blood-pres- 
sure is  elevated,  sometimes 
greatly,   above    the    normal. 


Hg. 
mm 

180 
170 
150 
150 
140 
130 
120 
110 
100 
90 
80 
70 


7 

17 

28 

3 

1 

6th 

2th 

(Edema 
Ascites 

tap 

oed 

_*> 

^ 

/ 

J 

'^' 

Fig.  42. — Blood-Peesstjee  Chart. 

F.,  aged  50:  IVIitral  disease;  cirrhotic 
kidney. 


This  is  shown  in  Fig.  42,  which  shows  the  pressure  in  a  patient, 
aged  fifty,  who  was  admitted  to  hospital  with  orthopnoea^ 
dropsy,  and  ascites,  in  whom,  with  improvement,  the  pressure 
rose  to  even  higher  levels. 

It  is  extremely  important  to  distinguish  between  these  two 
groups  of  cases.  In  aortic  stenosis,  and  in  both  the  mitral 
lesions,  the  blood-pressure  is  not  elevated  to  any  excessive 
degree,  no  matter  how  large  the  left  ventricle  may  be.  The 
hj-pertrophy  or  dilatation  is  exactly  calculated  to  compensate 
the  valvular  flaw,  to  insure  the  entrance  into  the  aorta  of  the 
normal  amount  of  blood,  and  to  maintain  the  aortic  blood- 


68 


DISEASES  OF  THE  HEART 


pre£  sure  at  normal  levels .  An  intrinsic  cardiac  lesion  (excluding 
aortic  regurgitation,  whose  effects  have  already  been  discussed) 
is  incapable  of  elevating  the  aortic  pressure,  and  the  presence 
of  a  high  blood-pressure  indicates  the  presence  of  some  ex- 


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trinsic  influence — an  intoxication,  renal  disease,   or  arterior 
sclerosis. 

The  converse  proposition  is  not,  however,  equally  true.  As 
one  would  expect,  an  elevated  blood-pressure  may  fall  to,  or 
even  below,  normal  from  mere  failure  of  the  vis  a  tergo.  The 
point  is  exemphfied  by  Fig.  43.     The  patient,  who  was  suffer- 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE  69 

ing  from  chronic  nephritis,  was  admitted  complaining  of  head- 
ache, vomiting,  and  dimness  of  vision.  The  radial  arteries  were 
thickened,  the  left  ventricle  was  enlarged,  and  the  ophthalmo- 
scopic picture  was  indicative  of  widespread  vascular  disease, 
and  included  several  examples  of  mihary  aneurism.  He  was 
kept  on  a  diet  of  milk  alone  from  May  14  to  June  18,  in  the 
hope  of  allaying  the  renal  mischief,  and  during  this  period  the 
pressure  steadily  fell,  ultimately  reaching  normal  or  perhaps 
subnormal  levels.  But  it  rose  again  on  the  resumption  of  a 
more  ample  dietary,  and  on  his  dismissal  was  distinctly  high. 
His  symptoms  were  in  complete  abeyance,  and  he  was  able  to 
take  a  fair  amount  of  exercise.  It  seems  clear  that,  in  this 
case,  the  blood-pressure  required  to  be  above  normal  on 
account  of  the  renal  and  arterial  disease,  and  that  the  normal 
pressure  on  June  18  was  due  to  cardiac  weakness  from  relative 
starvation.  There  were  no  symptoms  indicative  of  cardiac 
failure  at  this  time,  but  he  was,  of  course,  confined  to  bed,  and 
they  would,  I  suspect,  have  appeared  if  he  had  been  allowed 
out  of  bed.  He  again  came  under  observation  in  October, 
^vith  similar  symptoms,  and  a  systohc  blood-pressure  of  225- 
180  mm.  Hg.  Treatment  was  of  little  avail,  and  he  died  of 
uraemia  shortly  afterwards. 

In  those  cases  in  which  arterio-sclerosis  and  valvular  flaws 
co-exist,  a  correct  diagnosis  may  only  be  possible  from  observa- 
tion of  the  arteries,  the  puLse,  and  the  fundus  of  the  eye.  The 
cardiac  evidence  may  wholly  fail.  The  second  aortic  sound 
may  be  weakened  from  stiffness  of  the  cusps,  or  replaced  by 
miu-mur,  and  the  first  apical  sound  and  the  character  of  the 
apex  impulse  may  be  useless  as  guides.  It  should  be  remem- 
bered, however,  that  in  uncomphcated  mitral  disease  the 
second  aortic  sound  is  never  accentuated,  the  pulse  is  never 
hard  or  weU  sustained,  and  that,  with  failure,  the  apex  impulse 
becomes  weak,  diffuse,  and  of  short  duration. 

The  lesser  urcemic  manifestations  are  more  hkely  to  escape 
recognition  than  the  serious  symptoms,  for  the  latter  are 
usually  associated  with  well-marked  evidences  of  both  cardiac 
and  renal  disease ;  but  the  diagnosis  is  generally  definite  on  a 
careful  routine  examination.  The  symptoms  not  infrequently 
foUow  some   special   additional   intoxication,  often  due  to  a 


70  DISEASES  OF  THE  HEART 

gastro-intestinal  upset,  and  may  remain  for  long  in  abeyance 
if  circumstances  permit  a  mode  of  living  on  physiological  lines. 

Shortness  of  breath  is  a  symptom  of  which  arterio-sclerotic 
patients  frequently  complain,  and  requires  some  special  atten- 
tion, as  it  may  arise  in  several  ways. 

Emphysema  not  infrequently  occurs  in  middle-aged  people 
from  causes  which  are  apparently  trivial  in  their  character. 
A  cough,  which  is  not  necessarily  of  long  duration  or  of  great 
intensity,  and  may  never  have  seriously  inconvenienced  the 
patient,  may  be  the  only  apparent  cause.  But  it  will  often 
be  found,  in  such  cases,  that  the  pulse  is  hard,  the  arteries 
thick,  and  the  second  aortic  sound  accentuated.  The  lesion 
has  resulted  from  apparently  trivial  causes  on  account  of  the 
impaired  nutrition  produced  by  the  arterial  disease.  And  it 
is  often  combined  with  more  or  less  chronic  bronchitis,  which 
may  produce  symptoms  quite  out  of  proportion  to  the  in- 
tensity of  the  catarrh. 

Both  of  these  points  were  emphasized  recently  in  my  wards. 
Three  men  were  admitted  at  the  same  time,  suffering  from 
bronchitis.  One,  aged  forty-six,  had  been  liable  to  bronchitis 
for  many  years,  and  on  this  account  had  been  able  to  do  but 
little  work  during  the  three  preceding  winters.  His  chest,  as 
one  would  expect,  was  notably  emphysematous.  His  heart 
and  blood-pressure  were  normal.  Another,  aged  fift^-nine, 
who  was  almost  equally  emphysematous,  had  never,  he  said, 
been  ofi  work  previously  from  ill-health,  and  had  never  pre- 
viously suffered  from  bronchitis.  His  left  heart  was  consider- 
ably enlarged,  and  his  blood-pressure,  when  the  symptoms  had 
abated,  measured  175  mm.  Hg.  The  third  patient,  aged  thirty- 
eight,  had  no  emphysema,  and  the  pulmonary  symptoms  were 
not  grave ;  but  general  oedema  was  so  extreme  that  micturition 
was  difficult  from  the  tumefaction  of  the  prepuce  and  scrotum. 
Some  years  before  he  had  suffered  from  an  acute  nephritis, 
and,  although  the  renal  symptoms  were  trivial,  possessed  a  heart 
whose  apex  impulse  was  4|  inches  distant  from  mid-sternum. 

£n  another  group  of  cases  shortness  of  breath  is  related  to 
exertion,  and  is  evidently  due  to  relative  cardiac  insufficiency, 
even  though  the  pulse  is  full  and  hard,  and  the  left  ventricle 
hypertrophied  and  powerful. 


THE  SYMPTOMS  OF  ARTERIAL  DISEASE         71 

But  in  a  third  group  of  cases  the  dyspnoea  is  probably  toxic 
in  origin.  Cheyne-Stokes  respiration,  for  example,  occurs 
almost  exclusively  in  cases  of  nephritis  and  the  "  senile  " 
t3rpe  of  cardiac  disease,  and  is  then  present  in  the  class  of  case 
in  which  ehmination  is  likety  to  be  insufficient;  while  it  is 
conspicuously  absent  in  the  cardiac  failure  which  accompanies 
acute  endocarditis.  Cardiac  "asthma,"  too,  is  less  common 
in  the  latter  group  than  in  the  former,  and  primary  asthma, 
as  is  well  known,  is  not  infrequently  dependent  on  causes  of  a 
toxic  nature.  The  slighter  manifestations  of  dyspnoea  some- 
times own  a  similar  origin,  and  eliminative  treatment  should 
always  be  pursued  whenever  dyspnoea  is  nocturnal  or  paroxys- 
mal in  character,  or  of  a  severity"  which  seems  disproportionate 
to  the  other  evidences  of  cardiac  or  pulmonary  embarrassment.. 

It  is  impossible  to  enumerate  all  the  symptoms  which  may 
emerge  in  arterio-sclerosis.  Many  of  them  are  cerebral  (giddi- 
ness, faintings,  etc.),  many  are  peripheral  (cramp,  inter- 
mittent Hmp,  etc.),  many  are  visceral  (indigestion,  etc.),  while 
even  such  diseases  as  gastric  ulcer,  pancreatic  diabetes,  and 
enlargement  of  the  prostate,  have  been  considered  to  be  the 
result  of  arterial  disease.  It  seems  probable,  too,  that  in  some 
instances  the  proposition  is  accurate,  though  of  course  these 
symptoms  may  be  produced  by  very  different  pathological 
conditions . 

But  it  must  be  recognized  that  not  infrequently  in  middle- 
aged  and  elderly  people  there  is,  underlying  any  local  symp- 
tom which  may  require  attention,  a  widespread  general  disease 
— -arterio-sclerosis — a  disease  which  is  essentially  progressive, 
though  its  progress  may  be  delayed  by  suitable  treatment ;  and 
in  which,  quite  apart  from  any  special  lesion,  the  arteries  are 
everjrwhere  more  or  less  damaged,  the  cardiac  reserve  is  always 
lessened,  and  the  renal  functions  are  more  or  less  impaired. 

Arterio-sclerosis  is  no  new  disease.  It  is  "plethora  ";  it  is 
often  "renal  inadequacy  ";  it  is  often  "senile  heart  ";  it  is 
often  "goutof  the  aberrant  type  "and  the  "uric  acid  diathesis." 
In  many  cases  it  is  "  old  age,"  which  is  but  rarely  the  wearing 
out  of  undamaged  tissues,  and  too  generally  the  result  of 
physiological  misbehaviour  in  the  past — misbehaviour  which 
leaves  its  first  marks  upon  the  arteries.  — 


CHAPTER  IV 
THE  OCULAR  MANIFESTATIONS  IN  ARTERIO-SCLEROSIS 

By  Aethue,  J.  Ballantyne 

The  earliest  and  most  common  ophthalmoscopic  evidences  of 
arterio-sclerosis  in  the  retina  are  irregularities  in  the  calibre  of 
the  arteries  due  to  local  thickenings  of  the  intima,  and  con- 
striction of  the  veins  where  they  are  crossed  by  the  rigid 
arteries.  The  narrowing  of  the  arterial  lumen  is  sometimes 
more  uniform,  and  may  be  such  that  the  blood-columns  are 
reduced  to  mere  threads.  To  the  same  stage  belong  two 
other  conditions,  namely,  undue  tortuosity  of  the  arteries, 
and  an  excessive  brightness  of  the  central  light  streak,  which 
gives  to  the  arteries  the  so-called  "  silver-wire  "  appearance. 
Globular  or  fusiform  dilatations  of  the  arteries,  the  miHary 
aneurism,  may  also  be  found. 

The  walls  of  normal  retinal  vessels  are  inv'sible,  so  that  we 
see  only  the  blood-stream.  The  more  advanced  stages  of 
arterio-sclerosis  render  the  vessel  walls  visible.  The  first  evi- 
dence of  loss  of  transparency  of  the  wall  is  that  the  blood- 
column  looks  paler,  and  the  central  light-streak  less  striking 
than  normal.  At  a  later  stage  the  process  of  thickening  and 
degeneration  in  the  vessel  walls  proceeds  so  far  as  to  produce 
the  ophthalmoscopic  feature  described  as  "perivasculitis," 
the  blood-stream  being  bounded  on  each  side  by  a  clear  white 
line,  or  entirely  concealed  for  a  greater  or  smaller  part  of  ils 
course  by  a  dense  white  band,  which  represents  the  opaque 
wall  of  the  artery.  Bright,  glistening  spots  in  the  walls  of  the 
vessels  may  represent  deposits  of  lime  or  cholesterin. 

The  veins  may,  but  do  not  usually,  show  as  marked  changes 
as  the  arteries.  Constriction  of  the  veins,  where  crossed  by 
the  arteries,  has  already  been  mentioned.     In  the  more  ad- 

72 


THE  OCULAR  MANIFESTATIONS  73 

vanced  stages  the  veins  become  dilated  and  tortuous,  and 
may  show  irregularities  of  cahbre,  or  beading,  similar  to  those 
seen  in  the  arteries.  Excessive  prominence  and  tortuosity  of 
the  finer  venous  radicles  is  rather  a  characteristic  appearance. 

The  optic  nerve  also  alters  in  appearance.  It  becomes  con- 
gested, and  oedema,  either  confined  to  the  disc  and  to  its 
immediate  neighbourhood,  or  affecting  the  whole  of  the  retina, 
may  be  observed. 

Retinal  haemorrhages  are  common,  and  may  be  present  even 
when  the  only  visible  vessel  changes  are  irregularities  of  the 
arterial  cahbre  and  constriction  of  the  veins  by  the  arteries. 
With  or  without  retinal  haemorrhages,  we  may  see  white  spots 
and  patches,  due  to  retinal  degeneration.  These  occur  even 
in  the  absence  of  renal  disease,  and  it  is  indeed  uncertain 
whether  the  characteristic  changes  of  albuminuric  retinitis  are 
due  to  the  accompanying  vascular  changes,  or  whether  both 
are  attributable  to  the  one  underlying  cause. 

Besides  the  changes  described  in  the  retinal  vessels,  sclerosis 
of  the  choToidal  vessels  may  be  seen,  giving  the  appearance  of  a 
network  of  white  hnes  which  represent  the  opaque  vessel 
walls. 

Two  conditions  which  present  very  striking  and  characteristic 
ophthalmoscopic  pictures  may  be  referred  to  as  strong  evidence 
of  the  existence  of  local  vascular  disease.  These  are  obstruc- 
tion of  the  central  artery  of  the  retina  and  obstruction  of  the 
central  vein.  In  the  former  case  the  retina  at  the  posterior 
pole  of  the  fundus  presents  a  milky-white  opacity,  in  the  centre 
of  which  the  fovea  stands  out  as  a  bright,  cherry-red  spot. 
The  disc  is  pale,  the  arteries  are  reduced  to  threads,  and  the 
veins  are  also  somewhat  narrow.  While  these  appearances 
used  to  be  considered  characteristic  of  embolism  of  the  central 
artery  of  the  retina,  it  has  been  proved  that  in  many  cases  they 
are  brought  about  by  obstruction  of  the  artery  either  from 
endarteritis  or  from  endarteritis  flus  thrombosis.  Obstruction 
of  the  central  vein  of  the  retina  is  usually  caused  by  thrombosis 
associated  with  local  disease  of  the  vessel  wall.  On  ophthalmo- 
scopic examination  the  veins  are  seen  to  be  dark,  distended, 
and  tortuous,  the  arteries  are  narrow,  the  nerve  head  is  con- 
gested and   oedematous,   and   the  retina   contains   abundant 


74  DISEASES  OF  THE  HEART 

haemorrliages  and  wliite  exudative  patches.  This  condition 
is  apt  to  lead  to  destruction  of  sight  by  the  development  of 
glaucoma  (hsemorrhagic  glaucoma),  or  of  a  proliferative  retinitis. 

Other  ocular  evidences  of  angio- sclerosis  which  may  be  men- 
tioned are — the  slowly  progressive  optic  atrophy  which  some- 
times results  from  pressure  of  a  sclerosed  ophthalmic  artery  on 
the  optic  nerve  within  the  optic  foramen;  the  pupillary  dis- 
turbances due  to  sclerosis  of  the  vessels  of  the  iris,  and  those 
which  sometimes  accompam^  disease  of  the  aorta;  and  the 
visual  defects  which  result  from  focal  brain  disease  of  vascular 
origin. 

The  somewhat  rare  retinal  condition  called  "retinitis  cir- 
cinata  "  is  thought  by  some  to  be  due  to  disease  of  the  retinal 
vessels. 

The  plate  (Fig.  44)  illustrates  many  of  the  ocular  changes 
referred  to  in  the  accompanying  note.  It  represents  the  right 
fundus  ocuH  of  a  man  suffering  from  chronic  renal  disease.  There 
was  also  some  indistinctness  of  the  disc  margin  due  to  oedema, 
which  is  not  represented  in  the  drawing.  The  lower  temporal 
artery  is  undul}^  tortuous,  and  presents  the  "silver  wire" 
appearance  referred  to.  Three  months  before  this  drawing 
was  made  three  or  four  small  aneurisms  were  present  on  this 
artery  where  the  white  spots  are  now  seen.  A  branch  which 
leaves  the  same  artery  nearer  the  disc  passes  out  across  the 
fundus  as  a  white  opaque  streak.  The  upper  nasal  arter}' 
shows  sudden  and  marked  reduction  of  calibre  a  short  distance 
from  the  disc.  The  veins  on  the  whole  are  overdistended, 
and  are  seen  to  be  constricted  where  they  are  crossed  by  the 
arteries.  The  fine  terminal  twigs  are  abnormally  distended 
and  tortuous.  In  the  lower  inner  region  of  the  fundus  one 
of  these  twigs  shows  something  resembhng  an  aneurismal 
dilatation.  The  retinal  haemorrhages  and  white  spots  were 
much  larger  and  more  numerous  at  an  earlier  stage  of  the 
disease. 


CHAPTER  V 

THE  TREATMENT  OF  ARTERIO-SCLEROSIS  ^ 

The  treatment  of  arterio-sclerosis  is  essentially  preventive, 
and  thus  lies  to  the  hand  of  the  medical  attendant.  The  disease 
is  very  chronic,  and  one  in  which,  as  a  rule,  the  early  symptoms 
are  trivial,  though  serious  symptoms  may  develop  suddenly; 
and  even  when  the  shghter  manifestations  are  equivocal,  the 
underlying  condition  is  generaUy  apparent  whm  it  is  looked 
for.  And  if,  as  I  beheve,  Sir  Clifford  AUbutt's  theory  of  its 
origin  is  appKcable  to  a  large  number  of  cases,  its  develop- 
ment may  be  prevented,  or  at  any  rate  its  progress  may  be 
retarded  to  a  degree  which  as  yet  seems  scarcely  to  be  appre- 
ciated. But,  as  Huchard  weU  said,  the  treatment  is  a  regiine, 
and  not  a  drug,  and  a  regime  which  may  be  impossible  for 
a  busy  man  to  foUow;  and  in  such  cases  we  can  but  dehver 
to  our  patients  the  ultimatum  — a  radical  change  of  habits 
or  a  short  life— and  abide  by  the  decision  of  the  person  most 

concerned. 

The  introduction  of  the  Riva-Rocci  sphygmomanometer  into 
cHnical  work  naturaUy  evoked  the  hope  that  the  blood-pressure 
chart  would  supply  more  definite  indications  for  treatment 
than  had  hitherto  been  available,  but  a  very  short  experience 
sufficed  to  show  that  this  was  erroneous,  and  that  it  was  per  se 
an  unrehable  guide.  Onreflection,  too,  the  fallacy  was  obvious. 
In  acute  nephritis  the  blood-pressure  is  elevated  in  the  presence 
of  symptoms,  and  returns  to  normal  long  before  the  albuminuria 
has  disappeared.  But  in  those  forms  of  chronic  nephritis  with 
induration,  the  smaU  white  and  the  small  red  kidney,  the 
blood-pressure,  even  in  the  absence  of  symptoms,  never  runs 
at  a  normal  level.     Structural  changes  have  occurred,  and  the 

75 


76  DISEASES  OF  THE  HEART 

^  arteries  are  permanently  thickened ;  the  heart  is  permanently 
enlarged,  and  the  blood-pressure  is  permanently  elevated. 
And  just  as  the  amount  of  albumin  in  the  urine  is  an  unreliable 
guide  to  the  functional  activity  of  the  kidneys,  so  the  height 
of  the  blood-pressure  fails  to  reveal  the  degree  of  damage  that 
has  been  done  to  the  arteries  and  to  the  heart.  In  arterio- 
sclerotic patients  whose  elimination  is  even  relatively  insuffi- 
cient, the  blood-pressure  varies  considerably  from  apparently 
trivial  causes ;  a  mere  catarrh  may  suffice  to  elevate  it,  cardiac 
failure  may  lower  it,  and  every  nicety  of  examination  and  the 
most  careful  survey  of  the  case  may  for  a  time  prove  incapable 
of  solving  the  important  question  of  the  height  of  blood-pressure 
which  must  now  be  considered  "  normal  "  to  the  particular 
individual.  A  reading  of  180  mm.  Hg  may  be  too  low  for 
perfect  ehmination,  or  too  high  for  the  heart  to  cope  with 
successfully. 

Notwithstanding  these  strictures,  routine  estimation  of  the 
blood-pressure  and  a  daily  chart  are  of  great  value  in  guiding 
the  treatment  of  the  case.  Isolated  observations  are  of  little 
use,  particularly  those  taken  in  the  consulting-room,  where 
so  many  factors  (emotion,  fatigue,  etc.)  may  be  in  action,  pro- 
ducing a  variation  from  the  average  reading.  And  the  blood- 
pressure  chart  by  itself  is  equally  unreHable,  and  is  only  helpful 
when  it  is  taken  into  consideration  along  with  those  other  data 

A, jwhich  are  usually  available. 
^^  In  the  early  stages  of  the  disease  it  is  often  difficult  to  relate 
the  trifling  symptoms  to  their  exciting  cause,  and  as  it  is  more 
easy  to  discern  the  process  in  cases  where  the  symptoms  are 
well  marked,  the  latter  will  be  considered  first. 

The  onset  of  serious  symptoms  is  as  a  rule  more  or  less 
abrupt,  and  the  result  of  the  operation  of  some  new  factor.  A 
""^priori,  it  might  be  thought  that  the  onset  would  be  gradual 
in  response  to  the  steady  increase  in  the  grade  of  the  arterial 
lesions  or  the  renal  inadequacy,  or  the  gradual  diminution  of 
the  cardiac  reserve ;  but  such  a  course,  though  it  may  occur, 
is  distinctly  unusual.  The  minor  symptoms  occur  insidiousty, 
but  the  individual  is  curiously  tolerant  of  visceral  weaknesses 
of  gradual  onset,  and  instinctively  learns  to  protect  himself 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       77 


from  his  increasing  disabilities.  Business  responsibilities  are 
turned  on  to  younger  shoulders,  the  "  single  "  game  of  golf  is 
replaced  by  the  "foursome,"  alcohol  and  tobacco  are  thrown 
overboard  or  their  consumption  is  restricted,  and  a  quiet  life 
with  little  sudden  strain  permits  the  overtaxed  organs  to  per- 
form their  work  with  but  small  inconvenience  to  their  owner. 
There  is,  however,  little  or  no  reserve,  and  serious  symptoms 
result  from  conditions  which,  in  a  healthy  individual,  would 
occasion  no  anxiety. 

Bronchitis  is  a  common  cause  of  trouble.     Chronic  bron- 
chitis is  a  very  frequent  accompaniment  of  arterio-sclerosis, 
and  an  exacerbation  of  the 
catarrh  may  produce  symp-  >fc. 
toms  which  are  quite  out  of  ng. 

mm. 

proportion  to  the  intensity  jqo 
of  the  pulmonary  lesions.  ,90 
A  man  of  forty-seven  years, 
a  stonebreaker  by  occupa- 
tion and  an  alcoholic  by 
choice,  contracted  a  cold,  to 
which  he  at  first  paid  little 
attention.  A  week  later  he 
had  become  very  short  of 
breath,  and  his  feet  were 
swollen.  When  he  was  ad- 
mitted to  hospital  a  fort- 
night after  the  onset 
{Fig.  45),  oedema  was  uni- 
versal and  considerable. 
There  were  copious  albu- 
minuria and  sUght  hsema- 
turia,    and    a    well-marked 

bronchitis.  Within  the  next  ten  days  the  cedema  disappeared, 
and  he  lost  1  stone  IQi  pounds  in  weight,  the  albuminuria 
became  trivial,  and  the  bronchitis  subsided.  His  arteries  were 
tortuous  and  but  shghtly  thickened.  The  blood-pressure,  on 
admission  200  mm.  Hg,  fell  steadily  during  convalescence, 
and  soon  reached  subnormal  registers. 

The  illness  in  this  case  seemed  wholly  attributable  to  the 


180 
170 
160 
150 
140 
130 
120 
110 
100 
90 
80 
70 


12 

14 

16 

18 

21 

23 

25 

27 

30 

\ 

\ 

\ 

\ 

V 

•^ 

1 — « 

\ 

v 

N, 

V 

N 

\ 

V. 

■>.-, 

\ 

N 

^ 

\ 

V. 

^ 

^»^ 

Fig.  45. — Blood-Peessube  Chart. 

M.,  aged  47;  Chronic  nephritis  ;  bron- 
chitis; improvement. 


78 


DISEASES  OF  THE  HEART 


bronchitis,  which  was,  however,  associated  with  symptoms 
which  are  not  its  usual  accompaniments.  The  rapid  improve- 
ment in  the  renal  symptoms  negatived  the  diagnosis  of  an 
acute  nephritis,  and  suggested  the  irritation  of  an  already 
damaged  kidney,  an  inference  which  was  strengthened  by  the 
arterial  thickening  and  the  presence  of  a  white  patch  in  the 
retina  of  the  right  eye. 

Evidence  of  cardiac  failure  may  be  well  marked  in  these 
cases.  A  man,  aged  sixty-six,  who  was  habitually  intemperate 
and  suffered  from  a  chronic  cough,  contracted  a  fresh  bion- 
chitis.     He  became  very  short  of  breath,  and  had  to  be  propped 

up  in  bed  at  night,  and  suffered  from 
severe  pain  in  the  epigastrium. 
Within  a  week  he  was  forced  to  cease 
work  and  to  seek  admission  to 
hospital.  He  was  now  notably 
cyanosed  and  very  breathless,  re- 
quiring to  sit  almost  upright  in  bed. 
The  bronchitis  was  widespread,  and 
the  liver  was  enlarged  and  tender; 
the  feet  were  sKghtly  swollen,  and  the 
mitral  valve  was  incompetent.  The 
urine  contained  a  trace  of  albumin. 
Improvement  was  rapid,  and  he  was 
soon  lying  flat  in  bed,  while  the  apical 
murmur  and  the  enlargement  of  the 
liver  had  disappeared.  Coincidently 
the  blood  -  pressure  rose  from 
125-170  mm.  Hg  (Fig.  46).  The 
bronchitis  had  evidently  put  a 
strain  upon  an  already  overtaxed 
heart  which  it  was  unable  to  overtake,  and  the  consequent 
failure  was  severe  and  alarming. 

Excessive  indulgence  in  alcohol  may  produce  serious  symp- 
toms. A  tailor,  aged  fifty-one,  who  had  enjoyed  good  health 
prior  to  the  onset  of  the  symptoms  for  which  he  sought  advice, 
save  for  two  attacks  of  renal  disease,  one  at  the  age  of  twenty 
five,  following  scarlatina,  the  second  of  obscure  origin  at  the 
age  of  forty-one,  from  both  of  which  he  had  made  good  re- 


APRtL 

Hg 
mm. 

200 

190 
180 
170 
160 
150 
140 
130 
120 
110 
100 
90 
80 
70 

Fig, 


15 

20 

23 

28 

5 

^ 

^ 

/ 

/ 

/ 

r 

J 

46. — Blood-Pressure 
Chart. 


M.,  aged  66:  Bronchitis. 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS      79 

coveries,  took  one  day  drink  to  excess.  He  went  to  his  work 
next  morning,  but  about  three  o'clock  in  the  afternoon  was 
noticed  to  be  somewhat  stupid.  He  walked  to  the  door  to 
get  some  fresh  air,  and  soon  after  his  return  to  the  workshop 
became  unconscious  and  had  a  short  general  convulsion,  from 
which  he  rapidly  recovered.  His  blood-pressure  was  220-145 
mm.  Hg.  Six  weeks  later  he  again  got  drunk,  and  again 
had  a  convulsion;  and  a  fortnight  later  another  fit  occurred, 
this  time  apart  from  alcoholic  excess.  He  subsequently  be- 
came fairly  temperate,  and  the  convulsions  did  not  recur, 
but  he  "aged  "  rapidly  and  became  less  fit  for  work.  Two 
years  later  headaches  ensued,  and  he  had  to  leave  off  his  trade, 
and  in  a  few  months  succumbed  to  an  apoplectic  seizure  asso- 
ciated with  hemiplegia. 

Sepsis  is  another,  but  less  frequent,  cause.  A  man,  aged 
fifty-two,  who  had  probably  suffered  from  syphiHs,  and  had 
had  an  attack  of  nephritis  at  the  age  of  forty-six,  tore  the 
instep  of  his  foot  with  a  rough  boot-eyelet.  The  wound  sup- 
purated, and  was  poulticed.  A  week  later  the  other  foot  was 
found  to  be  swollen.  In  a  day  or  two  the  eyelids  became 
baggy,  and  he  complained  of  headache  and  of  frequency  of 
micturition.  He  was  very  breathless  too,  and  had  to  sit  up- 
right in  bed.  A  similar  origin  was  observed  in  a  man,  aged 
seventy-jSve,  whose  increasing  difficulties  had  been  carefully 
watched  for  some  years.  A  not  very  large  gumboil  formed 
about  a  carious  tooth,  and  he  was  fevered  for  twenty-four  hours 
until  it  was  evacuated.  But  general  symptoms  ensued,  and 
he  became  drowsy  and  mildly  delirious  and  extremely  weak, 
and  the  symptoms  only  subsided  slowly.  The  minor  forms  of 
sepsis,  particularly  those  associated  with  carious  teeth,  are 
probably  of  more  importance  in  this  respect  than  is  generally 
reahzed. 

Symptoms  not  infrequently  succeed  severe  haemorrhage, 
whether  gastric  or  intestinal,  or,  as  in  the  following  case, 
occurring  post-partum.  A  woman,  aged  thirty-five,  who  had 
always  been  healthy  save  for  an  attack  of  rheumatic  fever  at 
the  age  of  twenty,  which  kept  her  in  bed  for  three  months, 
noticed  that  her  feet  were  swollen  in  the  latter  half  of  her 
ourth  pregnancy.     Labour  was  difficult  and  prolonged  (twins), 


80 


DISEASES  OF  THE  HEART 


and  she  lost  much  blood.  The  oedema,  however,  rapidly  dis- 
appeared, and  she  felt  quite  well  when  she  got  up  out  of  bed 
on  the  ninth  day;  but  it  soon  recurred  and  became  extreme. 
She  was  now  (Fig.  47)  very  short  of  breath,  with  a  troublesome 
cough  and  spit ;  the  bowels  were  loose,  and  she  felt  sick  and 
vomited  on  several  occasions.  The  symptoms  steadily  in- 
creased in  severity,  and  she  died  three  months  later.  The 
strain  of  pregnancy  and  the  debihty  consequent  on  the  haemor- 
rhage proved  too  great  for  a  heart  which 
had  little  reserve  power. 

Starvation    often    produces     notable 
symptoms.     A  woman,  aged  sixty  years, 


NOV 


Hg. 
mm. 

210 


APRIL    1908        MAY 


JUNE 


JULY 


200 
190 
180 
170 
150 
rSO 
140 
130 
120 
110 
100 

90 

80 

70 

Fig.  48. — Blood-Pres- 
sure Chart. 

F.,  aged  60:  Cirrhotic 
kidney. 

who  was  in  extremely  poor  circumstances,  and  who  had 
been  starving  for  some  weeks,  noticed  that  her  feet  had 
become  swollen.  The  oedema  rapidly  involved  the  trunk 
and  face,  and  she  was  forced  to  stay  in  bed.  She  felt  sick, 
vomited  repeatedly,  and  was  very  short  of  breath.  The 
striking  feature  in  her  condition  on  admission  to  hospital  was 
the  emaciation.  The  muscles  were  tiny  and  soft,  the  skin 
was  dry  and  wrinkled,  and  the  subcutaneous  fat  was  minimal ; 
in  notable  contrast  with  a  full,  hard  pulse  and  a  blood-pressure 


Hg. 
mm. 

170 
160 

ISO 
140 
130 
120 

no 

100 
90 
80 
7Q 


17     25   1 

29 

7 

29 

8 

73 

77 

28 

3 

8 

\ 

k 

\ 

A 

V 

\ 

\ 

\ 

•v 

V. 

'^m^ 

^ 

\ 

\ 

\ 

Si^ 

"N 

V, 

j^ 

~* 

V 

^^ 

22 

25 

29 

26 

^ 

p.. 

— 

^, 

\^ 

DEC 


Fig.  47. — Bloou-Pressure  Chart. 

F.,  aged  35:  Mitral  disease;  cirrhotic  kidney.  Death 
on  July  23. 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       81 

of  190-135  mm.  Hg  (Fig.  48).  The  symptoms  subsided  as 
Ker  general  nutrition  improved,  but  the  blood-pressure  re- 
mained high. 

One  is  apt  to  forget,  when  treating  a  patient  with  a  local 
disease,  that  the  symptoms  may  be  due  to  a  general  condition, 
and  not  to  the  local  lesion,  although  both  the  prognosis  and 
the  treatment  depend  upon  the  correot  appreciation  of  the 
factors  which  are  producing  symptoms  at  the  particular 
moment.  When  symptoms  arise  insidiously,  the  outlook  is  as 
a  rule  more  serious  than  is  the  case  when  they  occur  as  the 
result  of  some  new  additional  factor,  for  the  lesions  are  usually 
already  advanced.  Speaking  generally,  the  immediate  prog- 
nosis in  private  practice  is  worse  than  among  hospital  patients, 
for  in  the  former  the  conditions  of  life  are  more  satisfactory 
and  the  breaking-strain  has  been  but  slight.  If  immediate 
recovery  occurs,  however,  the  prognosis  in  private  cases  is 
generally  the  better,  for  a  reasonable  life  of  leisure  is  usually 
unattainable  among  the  older  hospital  patients.  Their 
financial  position,  for  instance,  is  rarely  comfortable,  and  their 
alternative  lies  between  continuance  of  labour  and,  at  any  rate, 
relative  starvation  and  discomfort;  so  that  it  is  generally 
impossible  for  the  first  and  most  important  indication  for 
treatment — the  removal  of  the  cause  which  induced  the  occur- 
rence of  symptoms  and  the  prevention  of  its  repetition,  if 
that  be  possible — to  be  followed. 

The  symptoms  of  arterio-sclerosis  may  be  referable  to  the 
heart,  the  kidneys,  or  the  vessels. 

Cardiac  failure  produces  symptoms  similar  to  those  which 
occur  in  chronic  valvular  disease — shortness  of  breath,  oedema, 
etc. — and  in  the  main  the  comparison  is  exact.  In  some 
respects,  however,  a  difference  may  be  observed.  A  patient 
who  is  dying  from  the  cardiac  failure  of  pernicious  anaemia 
as  a  rule  hes  flat  in  bed,  and  is  rarely  orthopnoeic  even  when 
oedema  is  considerable  and  widespread.  Cases  of  serious 
failure  in  valvular  disease  in  early  life  may  have  notable 
distress  in  breathing,  and  may  have  to  sit  almost  upright,  but 
there  is  generally  some  special  adequate  reason  for  the  dyspnoea, 
bronchitis,  infarct,  or  pleural  effusion.     But  in  arterio-sclerosis 

6 


82  DISEASES  OF  THE  HEART 

dyspnoea  may  be  extreme  and  orthopncEa  absolute  without 
any  obvious  pulmonary  lesion,  though  of  course  such  a  con- 
dition ma}^  be  present,  and  then  intensifies  the  distress. 
Paroyxsmal  dyspnoea,  whether  of  the  asthmatic  or  Cheyne- 
Stokes  type,  rarely,  if  ever,  occurs  in  uncomplicated  cardiac 
disease ;  its  presence  seems  alwaj's  to  indicate  imperfect  elimina- 
tion, as  a  rule  of  renal  origin. 

The  chief  difficulty  in  the  treatment  of  these  cardiac  cases 
is  the  difficult}^  of  recognizing  the  precise  mode  of  the  failure, 
for  failure  ma 3"  occur  in  two  ways.  In  one  type  ehmination 
becomes  insufficient,  and  the  blood-pressure  is  in  conse- 
quence elevated  to  a  height  at  which  the  heart  is  unable 
to  work  easily.  In  the  other,  the  cardiac  failure  is 
primary. 

'  In  acute  nephritis,  as  is  weU  known,  the  blood-pressure  is 
higher  than  normal.  With  improvement  and  the  disappearanc  e 
of  symptoms  it  returns  to  the  normal  as  a  rule  long  before  the 
albumin  has  disappeared  from  the  urine.  In  art erio -sclerosis, 
on  the  other  hand,  the  blood-pressure  is  permanently  elevated. 
If  elimination  is  insufficient,  in  arterio-sclerosis,  as  in  acute 
nephritis,  the  blood-pressure  rises,  in  the  former  case  to 
extraordinary  heights,  and  the  heart  may  give  way  before  the 
extra  strain — a  mode  of  failure  which  is,  indeed,  well  known 
to  occur  occasionally  in  acute  nephritis.  But  we  do  not  know,, 
in  an  elderty  person  with  cardiac  failure  and  high  blocd-pressure, 
hoiv  inuch  of  the  latter  is  due  to  permanent  conditions  and  how 
much  to  tem'porary  causes,  unless  our  observations  have  been 
continuous  and  antecedent  to  the  onset  of  symptoms.  In 
arterio-sclerosis  the  permanent  elevation  of  pressure  gradually 
becomes  higher  as  time  rolls  on,  and  in  due  course  the  heart  wiU 
fail  before  its  task,  and  the  blood-pressure  will  fall,  sometimes 
very  considerabh',  with  the  onset  of  symptoms.  To  foUow 
the  weU-known  simile  of  the  horse  and  cart  of  coals  that  has 
stopped  on  a  hill,  we  are  in  doubt  whether  to  apply  the  whip 
or  to  hghten  the  load  so  as  to  enable  the  height  to  be  sur- 
mounted, and  we  have  often  to  pursue — tentatively  and  with 
care— both  courses. 

The  vagaries  of  blood-pressure  charts  are  extremely  curious,, 
and  their  interpretation  may  be  impossible  for  a  time. 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       83 


FEB 


A  baker,  aged  tliirtj'-eiglit,  was  admitted  to  hospital,  com- 
plaining of  headache,  nausea,  breathless ness,  and  swelling  of 
his  legs  and  body,  which  had  ensued  about  four  or  five  days 
previously,  coincident  with  the  onset  of  an  attack  of  bronchitis, 
to  which  he  was  subject  (Fig.  49).  The  left  heart  was  dilated, 
the  hver  enlarged  and  tender,  and  oedema  was  widespread 
and  considerable.  The  blood-pressure  was  elevated.  He  was 
given  a  dietary  of  milk,  evacuant  treatment  was  pursued,  and 
caffein  citrate  administered,  and  in  a  few  days  the  symptoms 
had  abated.  Coincidently  the 
blood-pressure  fell,  the  cliastohc 
fall  being  relatively  greater 
than  the  systohc.  The  bron- 
chitis seems  to  have  been 
responsible  for  an  increase  in 
the  blood-pressure  before  which 
the  heart  gave  way;  with  the 
subsidence  of  the  bronchitis  and 
cardiac  stimulation,  the  pres- 
sure fell  within  the  bounds  of 
the  cardiac  strength. 

Bronchitis,  as  is  well  known, 
imposes  extra  work  upon  the 
kidneys,  and  in  nephritis  even 
a  catarrh  may  produce  serious 
sjTuptoms.  A  striking  example 
occurred  recently  in  my  wards. 
A  man  who  was  convalescing 
from  nephritis  contracted  a 
catarrh  which  was  prevalent  in 
the  ward.  Coincidently  his  urine,  which  had  been  copious 
and  had  contained  a  mere  trace  of  blood,  became  scanty  and 
of  the  colour  of  porter.  The  chest  seemed  normal,  but  there 
was  a  cough  and  a  slight  muco-purulent  spit,  and  some  redden- 
ing of  the  fauces. 

In  the  baker's  case  cardiac  failure  occurred  before  an  acci- 
dental elevation  of  the  blood-pressure,  but  it  may  also  fail  before 
the  permanent  increase  of  pressure  due  to  arterial  disease,  as  in 
the  case  of  a  man,  aged  forty,  who  became  breathless  on  the 


JAN 

Hg. 
mm. 

210 

200 
190 
180 
170 
160 
150 
140 
130 
120 
110 
100 

90 

80 

70 

Fig 


21      ^3 

25 

27 

29 

1 

22 

\ 

X 

\ 

\ 

' 

* 

\ 

\ 

\ 

\ 

V. 

"^, 

49. — Blood-Pbessitee  Chart. 
M.,  aged  38:  Bronchitis. 


84  DISEASES  OF  THE  HEART 

least  exertion,  and  developed  oedema  of  his']  legs  whenever 
he  was  allowed  out  of  bed,  though  his  blood-pressure  was 
270-190  mm.  Hg. 

/'It  is  easy  to  lower  blood-pressure.  It  falls  notably  with  a 
sharp  attack  of  diarrhoea,  for  instance,  and  drastic  purgation 
and  a  restricted  dietary  can  almost  always  reduce  it  con- 
siderably. But  the  fall  is  not  necessarily  beneficial  to  the 
patient  if  it  results  from  cardiac  failure.  In  the  majority  of 
patients,  however,  in  the  presence  of  symptoms,  a  high  blood- 
pressure  indicates  imperfect  elimination,  and  care  should  be 
taken  to  insure  that  excretion  is  ample.  In  a  large  number  of 
cases  relief  occurs. 

A  high  blood-pressure  in  arterio-sclerosis  is  not  necessarily 
an  index  of  intoxication,  for  in  this  disease  the  blood-pressure 
is  always  elevated,  and  the  "  normal  "  pressure  is  that  at 
which  the  heart  works  easily  and  elimination  is  sufficient — 
i.e.,  the  pressure  at  which  symptoms  are  in  abej-ance — and 
it  can  only  be  gauged  by  repeated  observations  over  long 
periods  of  time. 

Vasodilator  drugs  have  been  much  lauded  and  much  depre- 
ciated at  different  times.  There  is  little  use  in  giving  them 
to  a  patient  whose  ehmination  is  insufficient  and  peripheral 
resistance  in  consequence  increased;  we  are  giving  with  one 
hand  and  taking  away  M'ith  the  other;  and  they  can  have 
but  little  action  upon  fibroid  vessels.  Their  chief  value  is  in 
temporary  emergencies,  and  their  continued  use  in  patients 
who  are,  so  to  speak,  convalescent  is  a  confession  of  failure — 
our  failure  to  insure  that  elimination  is  sufficient  in  the  par- 
ticular case. 

The  action  of  the  digitalis  series  in  cases  of  arterio-scleiosis 
when  cardiac  failure  has  supervened  is  in  the  majority  of 
patients  injurious,  and  the  dyspncea  is  intensified  and  the 
venous  stasis  increased.  The  special  cardiac  functions,  too, 
may  be  disturbed,  and  an  irregular  pulse  may  give  evidence  of 
a  hitherto  latent  heart-block  or  an  excessive  excitabihty;  or 
the  pulsus  alternans  may  occur.  Caffeine,  diuretin,  alcohol, 
and  the  ammonium  salts  are  more  generally  useful,  and  should 
be  tried  first,  and  should  be  aided  by  the  milder  diuretics, 
such  as  the  citrate  or  acetate  of  potassium,  and  liquor  ammonii 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS        85 


JUNE 


acetatis.  Strong,  freshly  infused  tea  and  coffee  are  often  usetul. 
But  it  must  be  acknowledged  that  in  many  instances  these 
drugs  prove  useless,  and  we  are  forced  to  resort  to  the  digitalis 
group. 

French  writers  advocate  isolated  massive  doses  in  cardiac 
failure,  but  the  repeated  administration  of  small  doses  seems 
preferable  in  the  cases  which  we  are  now  considering,  as  the 
minor  adverse  symptoms  can 
then  be  quickly  checked  by 
thejvithdrawal  of  the  drug. 
A  standardized  tinctui'e,  the 
Nativelle  granules,  Trous- 
seau's wine,  or  Guy's  pills, 
may  be  utihzed ;  the  granules 
and  the  wine  scarcely  ever 
upset  the  stomach.  Some 
patients  are  very  susceptible 
to  mercury,  and  I  have  seen 
well-marked  salivation  occur 
after  the  administration  of 
fourteen  Guy's  pills  in  seven 
days.  Oral  sepsis  was  ex- 
treme in  this  patient,  but  the 
use  of  mercury  should  always 
be  carefully  watched  in  these 
cases,  particularly  if  the  renal 
functions  are  also  notably 
disturbed. 

The  actual  height  of  the 
blood-pressure  is  a  matter  of 
no  practical  importance,  and 
I  have  given  even  large  doses 


MAY 

Hg. 
mm. 

250 
250 
240 
230 
220 
210 
200 
190 
180 
170 
160 
150 
KO 
130 
120 
110 
100 
30 
80 
70 


7 

6 

12 

18 

31 

13 

23 

26 

r 

/ 

1 

1 

' 

J 

/ 

/ 

/ 

I 

/ 

J 

Fig.  50. — Blood-Peesstjre  Chart. 
F.,  aged  58:  IVIitral  disease;  cirrhotic  kidney. 


of  digitalis  in  high-pressure  cases  with  benefit.  A  woman,  aged 
fifty-eight,  was  admitted  to  hospital  orthopnoeic  and  very 
short  of  breath,  with  extensive  oedema  and  a  large  effusion 
into  the  left  pleural  sac  (Fig.  50).  Paroxysmal  attacks  of 
dyspnoea  occurred  at  night.  The  effusion  had  to  be  tapped 
on  five  occasions,  but  she  left  hospital  after  two  months' 
residence,  fairly  comfortable  and  \vithout  any  oedema,  though 


86 


DISEASES  OF  THE  HEART 


she  was  short  of  breath  when  she  was  walking  about.  Coin- 
cident with  the  improvement,  the  blood-pressure  rose  from 
160-250  mm.  Hg.  The  improvement,  however,  was  of 
short  duration,  and  she  returned  to  hospital  in  a  moribund 
condition  two  months  later. 

The  height  of  the  blood-pressure  is  no  index  to  cardiac  suffi- 
ciency. A  man,  aged  sixty-eight,  was  admitted  to  hospital 
two  days  after  the  occurrence  of  a  right-sided    hemiplegia 

(Fig.  51).  Three  days 
later  he  was  more  stupid 
than  on  admission, 
deglutition  was  difficult, 
and  incontinence  of  urine 
complete,  and  the 
breatliing  was  typically 
Chej'ne-Stokes  in  char- 
acter and  associated 
with  pupillary  and  pulse 
phenomena.  The  ex- 
tremities were  cold  and 
blue.  Three  days  later, 
when  improvement  was 
distinct,  the  blood-pres- 
sure was  practically  the 
same,  although  all  the 
evidences  of  venous 
stasis  had  passed  away. 
It  is  difficult  to  realize 


DEC 

Hg. 

mm. 

210 
200 
190 
180 
170 
160 
150 
HO 
130 
120 

no 

100 
30 
80 
70 


12 

13 

?4 

15 

16      17 

18 

79 

20 

21 

"A 

\ 

\ 

\ 

V 

■n 

\ 

\/ 

\ 

\ 

V 

^ 

\ 

\ 

v 

^ 

-■•^v, 

N.^ 

^ 

Fig.  51. — Blood-Peessxtre  Chart. 
M.,  aged  68:  Hemiplegia. 

that  cardiac  failure  may  be  present  with  a  blood-pressure  of 
over  150  mm.  Hg,  but  improvement  ensued  after  the  adminis- 
tration of  strong  tea  and  whisky  and  a  more  ample  dietary — 
treatment  which  could  hardly  have  any  great  effect  upon  a 
gross  cerebral  lesion.  In  another  case  the  demonstration  was 
more  complete.  The  patient,  a  man  aged  fifty-one,  who  was 
suffering  from  renal  cirrhosis,  developed  cerebral  symptoms 
which  the  post-mortem  examination  showed  were  the  result  of 
cortical  emboli  derived  from  clots  in  the  left  ventricle.  His 
blood-pressure  had  ranged  from  170  to  210  mm.  Hg. 
'"  In  many  of  these  cases  of  cardiac  failure  the  whip  is  not 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       87 

required,  for  if  some  of  the  coals  be  removed  from  the  cart, 
the  bm-den  can  be  borne,  and  with  adequate  rest  the  heart 
regains  its  strength. 

Cases  with  symptoms  of  urcemic  type  react  well  to  treatment 
of  this  kind.  Free  purgation,  packs,  cupping,  and  an  ample 
supply  of  fluid  are  the  main  elements  in  treatment,  and  the 
cardiac  dilatation  often  rapidly  subsides,  and  the  pulse  becomes 
less  frequent.  The  administration  of  water  is  important.  It 
can  often  be  retained  when  any  food  is  at  once  ejected,  and, 
of  course,  can  be  given  subcutaneously  or  by  the  bowel.  Con- 
tinuous rectal  injections,  as  practised  by  surgeons  after  ab- 
dominal operations,  are  sometimes  useful.  But  here  again 
the  behaviour  of  the  blood-pressure  varies. 

As  a  rule,  with  increased  elimination  and  the  disappearance 
of  symptoms,  the  blood-pressure  falls.  This  is  well  shown  in 
Fig.  52 — that  of  a  man,  aged  thirty-six,  who  was  admitted 
suffering  from  chronic  nephritis,  and  complaining  of  headache, 
vomiting,  and  dimness  of  vision.  On  a  diet  of  milk  and 
ehminant  treatment  the  symptoms  rapidly  subsided  and  the 
blood-pressure  fell,  though  it  rose  again  on  the  resumption  of  a 
more  ample  dietary. 

But  the  fall  in  pressure  may  be  slight  even  when  improve- 
ment occurs.  A  woman,  aged  45,  terminated  her  eleventh 
pregnancy  prematurely  in  January.  In  June  she  began  to 
suffer  from  headache,  which  steadily  became  more  severe  and 
persistent,  and  at  times  prevented  sleep.  Nausea  and  vomit- 
ing ensued  in  December,  and  in  January  was  very  severe, 
almost  all  food  being  rejected  at  once.  On  admission,  in 
February,  she  was  extremely  ill,  with  a  pale,  anxious  expression, 
yawning  continually,  and  complaining  bitterly  of  headache 
and  nausea  (Fig.  53).  For  forty-eight  hours  after  admission 
she  vomited  almost  constantly,  but  the  symptoms  afterwards 
improved  rapidly,  and  she  left  hospital  in  fair  health.  The 
blood-pressure  in  this  case  fell  at  first,  but  rose  again  before 
dismissal.  Treatment  was  eliminant,  and  she  was  able  to 
retain  even  large  quantities  of  water  in  the  stomach  at  a  time 
when  all  varieties  of  food  were  at  once  rejected. 

The  blood-pressure  may  even  rise  under  similar  treatment. 
A  woman,  aged  forty-six,  who  had  suffered  from  rheumatic 


88 


DISEASES  OF  THE  HEART 


fever  in  early  life,  began  to  be  troubled,  about  the  age  of  thirty- 
eight,  with  breathlessness  and  palpitation,  and  became  subject 
to  attacks  of  bronchitis.  Six  years  later  oedema  made  its 
appearance,  at  first  in  the  face  and  then  in  the  feet,  and  nausea 
and  vomiting  ensued.     When  she  was  admitted  to  hospital  a 


Ol 

1 

I    1 

s. 

k^ 

en 

'V 

1 

\ 

^~" 

\ 

7 

V 

M 

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year  afterwards,  there  was  slight  general  cedema  and  a  small 
ascitic  collection,  and  she  was  emaciated  and  weak  (Fig.  54, 
March,  1908).  Rest  in  bed,  a  milk  diet,  and  increased  elimina- 
tion rapidly  dissipated  all  the  symptoms,  and  coincidently 
the  blood-pressure  rose  from  155  to  175  mm.  Hg.     The  only 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       89 


stimulant  administered  was  some  Easton's  syrup.  The  further 
history  is  instructive.  The  symptoms  recurred,  and  she  was 
readmitted  into  hospital  with  similar  but  more  severe  symp- 
toms. On  this  occasion  Trousseau's  wine  was  given,  and  she 
made  a  slow  recovery,  and  again  the  blood-pressure  rose  from 
150  to  175  mm.  Hg.  She  was  again  admitted  to  hospital, 
sixteen  months  after  dismissal.  The  blood-pressure  was 
then  140  mm.  Hg,  and 
treatment  failed  to  pro- 
duce any  distinct  improve- 
ment, the  blood-pres- 
sure remaining  practically 
constant.  Post-mortem 
examination  revealed  the 
widespread  nature  of  the 
disease,  for  there  was 
found,  besides  mitral 
stenosis  and  thickened 
degenerate  vessels,  well- 
marked  cirrhosis  of  the 
kidneys  and  pulmonary 
emphysema,  and  an  early 
cirrhosis  of  the  liver. 

In  the  milder  forms  of 
cardiac  failure,  then,  elimi- 
nant  treatment  is  the  main 
indication,  and  not  infre- 
quently is  sufficient  in 
itself  to  relieve  the  symp- 
toms, but  in  more  severe 
failure  cardiac  stimulants 
may  be  required  in  addi- 
tion. The  essential  point  in  treatment  is,  however,  improved 
elimination ;  without  it  stimulation  is  frequently  unsuccessful. 

The  arterial  lesions  in  arterio-sclerosis  are  often  serious,  and 
the  urgency  of  the  local  lesion  is  apt  to  distract  attention  from 
the  underlying  cause.  In  aneurism  and  in  cardiac  and  renal 
cases  the  condition  of  the  vessels  is  investigated  as  a  matter 
of  routine;  but  in  many  other  diseases,  such  as   epistaxis. 


FEB 

6 

8 

JO 

12 

14 

16 

18 

20 

21 

Hg. 

mm. 

A 

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70 

Fig.  53. — Blood-Peessuee  Chaet. 
F.,  aged  45:  Chronic  nephritis. 


90 


DISEASES  OF  THE  HEART 


gastric  ulcer,  etc.,  in  which  arterial  lesions  are  only  occasionally 
the  cause,  their  condition  is  apt  to  be  neglected,  though  the 
bearing  upon  treatment  is  necessarily  considerable. 

There  has  been  much  diversity  of  opinion  as  to  the  rela- 
tionship between  aneurism  and  heightened  blood-pressure,  a 
diversity  which  is,  in  part  at  any  rate,  due  to  erroneous  deduc- 
tions from  the  available  facts.  The  blood-pressure  is  measured 
in  the  brachial  artery,  which  is  a  branch  of  the  subclavian. 
It  is  manifest  that  the  blood-pressure  in  the  subclavian  artery 
cannot   be  high   if  a   distensible  aneurismal  sac   intervenes 


JUN 

DEC 

MAR 

}2 

25 

MAr 

7 

17 

28 

3 

NOV 

20 

25 

29 

19 

US 

He- 

mm. 

190 

09 

180 

170 

/ 

^ 

^ 

160 

J 

/ 

f 

150 

/ 

/ 

130 

•v 

^ 

120 

1 1 0 

100 

/ 

/ 

^ 

90 
80 

7n 

Fig.  54. — Blood-Pbesstjre  Chart. 
F.,  aged  46:  Mitral  disease;  cirrhotic  kidney. 

between  it  and  the  heart ;  while,  on  the  other  hand,  an  abdom- 
inal aneurism  will  not  influence  the  subclavian  pressure.  In 
cases  of  aortic  regurgitation,  too,  the  aortic  blood-pressure 
depends  largely  on  the  degree  of  the  incompetence,  and  the 
aortic  valves  are  often  affected  in  cases  of  aneurism.  But  all 
cases  of  aneurism  are  combined,  and  a  general  conclusion  is 
stated  which  has  been  based  upon  a  collection  of  facts  which 
are  not  truly  comparable. 

A  similar  error  has  been  made  in  regard  to  organic  mitral 
disease,  and  the  pulse  has  been  stated  to  be  hard  or  soft,  large 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS      91 

or  small,  regular  or  irregular,  by  various  writers.  The  frequent 
association  of  chronic  renal  disease  and  mitral  stenosis  has 
been  recognized  for  many  years  in  the  post-mortem  room,  but 
the  chnical  appHcation  of  this  fact  seems  to  have  escaped 
notice.  There  are  two  kinds  of  mitral  disease,  as  G.  A.  Gibson 
said — those  with  low  arterial  pressure  and  those  with  high 
pressure — and  the  difference  lies  in  extracardiac  lesions  in  the 
arteries  and  in  the  kidneys.  In  the  second  group  these 
systems  are  more  or  less  involved ;  in  the  first  they  are  normal 
(c/.  Figs.  41,  42,  and  p.  269). 

The  treatment  of  arterio-sclerosis  in  the  early  stages,  when 
the  symptoms  are  obscure  and  slight,  is  most  important,  for 
it  is  then  that  its  effect  is  greatest,  not  only  in  the  relief  of 
symptoms,  but  in  arresting  the  progress  of  the  disease. 

The  general  indications  have  aheady  been  laid  down.  The 
blood-pressure  is  elevated  by  the  presence  of  various  dele- 
terious substances  in  the  blood.  Continued  high  pressure 
produces  permanent  structural  alterations  in  the  heart  and 
bloodvessels — arterio-sclerosis.  In  every  case  of  arterio- 
sclerosis renal  ehmination  is  more  or  less  insufficient,  the  cardiac 
reserve  is  lessened,  the  viscera  are  poorly  nourished,  and  their 
functions  are  imperfectly  discharged. 

There  is  a  general  consensus  of  opinion  that  a  generous  diet 
and  excessive  consumption  of  alcohol  lead  in  time  to  "  plethora" 
and  increased  arterial  pressure.  Sir  Clifford  AUbutt  has 
crystallized  this  in  his  statement  that  the  most  important 
cause  is  "  repletion,  relative  or  positive — i.e.,  tempered  or  un- 
tempered  by  air  and  exercise,"  hindering  the  capillary  flow, 
and  augmenting  the  arterial  blood-pressure.  It  seems  prob- 
able that  Sir  CUfford  AUbutt 's  theory  is  appHcable  to  many 
cases,  the  type  of  which  is  the  big,  burly  individual,  energetic 
in  aU  his  habits,  and  overburdened  with  adipose  tissue.  But 
the  disease  is  not  uncommon  in  quite  another  type,  under- 
average  in  size  and  weight,  of  sedentary  habit,  and  from  cir- 
cumstances or  choice  exceeding  neither  in  eating  or  drinking. 
William  Russell  has  suggested  the  probable  explanation.  It  is 
not  the  quantity  of  the  food  that  is  at  fault  in  these  patients, 
but  imperfect   digestion.     The  primary   error   may   be   very 


92  DISEASES  OF  THE  HEART 

varied,  an  injudicious  choice  of  food,  gastric,  intestinal,  hepatic, 
or  pancreatic  insufficiency ;  but  the  ultimate  result  is  the  same — ■ 
imperfect  and  disturbed  metabolism  and  persistent  intoxica- 
tion. 

The  kidneys  are  mainly  concerned  with  the  removal  of  the 
waste  products  of  protein  metabolism.  If  this  be  excessive, 
their  functions  ma 3^  be  overtaxed ;  if  it  be  abnormal,  abnormal 
substances  may  be  formed  and  excreted  in  the  urine  {e.g., 
sugar,  indican,  etc.),  and  there  is  evidence  that  most  of  these 
bodies  irritate  the  kidneys  during  their  excretion.  Under 
normal  conditions,  carbohydrate  and  fat  metaboHsm  impose 
Uttle  work  upon  the  kidneys,  unless  their  consumption  be 
excessive  {e.g.,  aHmentary  glycosuria),  but  in  disease  their 
metabolism  may  be  imperfect,  and  the  products  may  be 
excreted  in  the  urine  {e.g.,  sugar,  acetone  series,  oxalates,  etc.). 

In  a  general  way  the  intake  of  food  must  be  carefully  super- 
vised and  excess  avoided,  and  a  minimum  of  protein  food 
allowed.  But  the  proverb,  "  One  man's  meat  is  another  man's 
poison,"  is  peculiarly  apphcable  to  arterio-sclerotic  patients, 
and  a  failure  of  digestion  and  the  consequent  irritation  of  the 
tissues  from  the  presence  of  injurious  substances  in  the  blood 
may  lead  to  the  occurrence  of  serious  symptoms. 

Appetite,  for  instance,  is  probably  essential  to  perfect  diges- 
tion, and  may  fail  before  the  "simple  hfe  and  food."  Vege- 
tarian diet  is  weU  recognized  to  be  difficult  of  digestion,  and  the 
glass  of  wine  at  meals,  or  savoury  dishes,  may  be  necessary 
stimulants  for  the  individual.  If  digestion  is  imperfect,  the 
undigested  foodstuffs  in  the  bowel  may  ferment  or  putrefy, 
and  a  new  series  of  irritant  materials  may  become  available 
for  absorption.  As  a  result  of  "fermentative"  processes, 
acetic,  lactic,  propionic,  butjTic  acids,  etc.,  may  be  formed; 
while  from  protein  "putrefaction,"  neurin,  chohn,  putrescin, 
cadaverin,  mercaptan,^_  HgS,  phenol,  cresol,  skatol,  indol,  etc, 
may  be  produced. 

This  point  dees  not  seem  to  have  been  sufficiently  recog- 
nized, perhaps  because  the  effects  of  indigestion  vary  so  greatly 
even  when  the  digestive  disturbances  are  apparently  com- 
parable. But  in  one  patient  a  bout  of  vomiting  or  an 
attack  of  diarrhoea  may  rapidly  remove  the  irritant,  while  in 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       93 

another  headache,  depression,  irritabihty,  etc.,  show  that 
absorption  has  occurred.  There  is  no  exact  relationship  be- 
tween the  amount  available  for  absorption  and  that  actually 
absorbed ;  for,  as  Herter  has  shown,  indicanuria  may  be  well 
marked  when  the  faecal  indol  is  inconsiderable,  and  insig- 
nificant when  the  latter  is  excessive. 

A  suitable  dietary,  then,  cannot  be  rigidly  laid  down  with- 
out considerable  experiment.  It  is  important  to  make  changes 
slowly,  and  to  regard  the  general  condition  of  the  patient  as  a 
whole.  One  is  apt  to  limit  the  amount  of  food  too  strictly, 
and  the  latter  error  may  be  as  injurious  as  overfeeding.  But 
no  diet  is  suitable  unless  the  tongue  is  clean,  gastro-intestinal 
symptoms  wholly  absent,  and  the  stools  normal  in  colour  and 
odour  and  consistence. 

The  "output  "  in  these  cases  is  quite  as  important  as  the 
"intake,"  and  requires  equal  attention.  A  daily  evacuation 
of  the  bowels  may,  for  instance,  be  insufficient,  and  I  have 
more  than  once  been  able  to  feel  the  colon  throughout  its 
course,  though  the  bowels  moved  regularly  every  day.  In 
some  of  these  cases  regular  laxative  medicine  may  be  required, 
in  others  only  occasional  doses;  but  the  weekly  "wash-out  " 
is  probably  alwa^-s  salutary  even  when  it  seems  unnecessary. 
The  kind  of  drug  employed  is  of  less  importance  than  the 
thoroughness  of  the  process.  My  own  preference  is  for  a  mer- 
curial, in  particular,  blue  pill,  with  a  saline  as  the  occa- 
sional purge,  and  the  milder  salines,  cascara,  or  senna,  for 
regular  use. 

The  kidneys,  too,  require  regular  flushing.  A  simple  di- 
uretic mixture  is  often  helpful,  but  it  should  be  subservient 
to  the  ingestion  of  water  in  amount,  the  daily  output  of  urine 
being  kept  over  60  ounces.  But  here,  again,  care  is  necessary, 
for  the  "  long  "  drink  at  meals  is  not  unhkely  to  disturb 
digestion.  Fluid  should  be  taken  when  the  stomach  is  empty, 
the  first  thing  in  the  morning,  a  full  half-hour  before  luncheon 
and  dinner,  and  perhaps  at  bedtime. 

The  skin,  too,  must  be  kept  active.  A  Turkish  bath  once 
or  twice  a  week  is  often  well  borne,  but  regular  toilet  ablutions 
and  mild  sweating  exercises  are  probably  a  better  substitute; 
and  many  amusements  may  be  utilized — golf,  riding,  tennis, 


94  DISEASES  OF  THE  HEART 

shooting,  fishing,  etc. — if  they  are  available,  and  of  a  degree 
adapted  to  the  physique  of  the  particular  individual. 

In  the  treatment  of  an  individual  patient  it  is  generally  wise 
to  insist  at  the  outset  upon  a  strict  regime.  The  details  are 
thus  better  learnt,  and  as  the  symptoms  remit,  relaxations  can 
be  readily  allowed,  while  an  increase  of  the  restrictions  after 
a  period  of  treatment  is  naturally  disappointing  to  the  patient. 

In  any  case  where  the  symptoms  are  severe,  confinement  to 
bed  is  generally  advisable  at  first.  The  bowels  should  be  kept 
freely  open  by  salines  and  blue  pill,  the  fluid  intake  increased 
so  that  60  to  90  ounces  of  urine  are  passed  per  diem,  and 
ehmination  assisted  by  a  simple  diuretic  mixture.  The  skin 
should  be  kept  active  by  a  daily  warm  bath,  and  the  diet 
restricted  to  three  or  four  pints  of  milk,  with  or  without  the 
addition  of  some  farinacea.  Milk  is  usually  weU  borne  by 
these  patients ;  if  there  is  any  digestive  discomfort,  it  can  be 
overcome  by  peptonizing  or  citrating  the  milk,  or  by  giving 
it  as  curds  or  "soured."  As  a  rule  the  symptoms  rapidly 
subside  as  soon  as  excretion  is  ample.  But  restrictions  of  this 
kind  cannot  be  maintained  for  long  with  benefit,  and  in  the 
absence  of  symptoms  some  addition  should  be  made  to  the 
diet  after  a  few  days.  The  quantity  of  farinacea  is  increased, 
and  white  fish  and  eggs  are  given  in  addition,  but  their  amount 
must  at  first  be  limited  and  only  gradually  augmented.  The 
cooking  must  be  of  the  plainest  kind,  but  every  possible 
variation  should  be  used,  so  as  to  encourage  appetite  and 
promote  digestion.  In  the  majority  of  cases  improvement 
continues,  and  the  diet  may  then  be  still  further  varied  by 
the  inclusion  of  chicken  and  rabbit  and  a  little  potato.  The 
key  to  treatment  at  this  stage  is  the  condition  of  the  digestive 
functions  and  the  general  well-being  of  the  patient  rather 
than  the  height  of  the  blood-pressure  or  the  amount  of  albumin 
in  the  urine. 

Some  digestive  help  may  be  required — some  rhubarb  or  soda, 
or  a  pepsin  mixture — and  the  tongue  must  be  clean,  the  stools 
normal,  and  gastro-intestinal  symptoms  in  abeyance  before  any 
notable  addition  to  the  diet  is  made.  Digestive  disturbances 
are  not  infrequently  the  result  of  oral  wrongdoing,  and  every 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       95 

effort  should  be  made  at  the  outset  to  insure  that  oral  sepsis  is 
absent,  and  that  efficient  mastication  is  possible ;  and  the 
patient's  attention  should  be  drawn  to  the  necessity  that  it 
should  be  thorough  and  complete. 

Mild  massage  may  be  commenced  at  this  stage  as  a  pre- 
liminary to  a  certain  amount  of  exercise,  and  the  latter,  when 
permitted,  must  be  supervised  at  first  by  the  physician  as 
sedulously  as  it  is  done  in  a  sanatorium,  for  tuberculous  patients, 
for  the  general  feeling  of  weU-being,  often  coupled  with  a  loss 
of  superfluous  fat,  is  apt  to  incline  the  patient  to  an  amount 
of  physical  exertion  which  is  too  great  for  his  flabby  muscles. 

There  is  always  difficulty  in  regulating  these  details  when 
a  return  to  work  is  finally  allowed,  for  the  exigencies  of  busi- 
ness necessarily  interfere  with  the  placid,  orderly  routine  of 
life  wliich  is  so  essential  to  an  arterio-sclerotic  patient.  The 
daily  time-table  must  be  laid  down  by  the  physician,  and  par- 
ticular care  taken  that  the  meals  are  regular  and  of  suitable 
quality;  and  that  some  rest  is  possible  both  before  and  after 
them . 

The  diet  in  convalescence  is  often  restricted  within  too  narrow 
limits.  The  cause  of  the  disease  is  often  dietetic,  and  the 
error  ma}^  arise  in  different  ways.  In  one  case  it  is  the  quantity 
of  food  that  is  at  fault,  in  another  the  quahty ;  while  in  a  third 
both  of  these  factors  may  be  satisfactory,  and  the  error  lies  in 
faulty  digestion.  It  is,  of  course,  manifest  that  all  foods  which 
are  notoriously  difficult  of  digestion  (crab,  goose,  etc.)  or  decom- 
posing (high  game)  must  be  avoided,  as  well  as  all  salted  foods, 
for  it  is  notorious  that  the  excretion  of  salt  is  almost  always 
defective.  The  red  meats  are  usually  interdicted.  In  a  general 
way  they  are  as  easil}'  digested  as  the  white,  and  contain 
httle  more  extractives ;  but  they  are  essentially  the  savoury 
foods,  and  so  Hkely  to  encourage  overeating;  and  they  are 
often  spiced  and  salted  in  the  cooking  to  a  degree  that  must 
entail  considerable  strain  on  elimination.  The  ordinary  con- 
soTrnne,  for  example,  contains  a  minimum  of  nourishment  and  a 
maximum  of  substances  to  be  excreted  by  the  kidney,  so  that 
aU  soups  made  with  meat  stock  should  be  prohibited.  Vege- 
table stock,  however,  may  be  utihzed. 

A  little  roasted  mutton  or  a  lightty  shot,  fresh  young  bird 


96  DISEASES  OF  THE  HEART 

is,  however,  certainly  permissible  as  an  occasional  variation. 
The  viscera  are,  of  course,  objectionable  on  account  of  their 
purin  content.  The  vegetables  only  require  consideration  from 
the  digestive  point  of  view,  and  the  majority  of  the  fruits  can 
be  allowed  in  their  season. 

The  use  of  drugs  in  arterio-sclerosis  requires  some  further 
consideration.  There  is  no  specific  medicine,  and  the  essential 
fart  of  the  treatment  is  the  regulation  of  the  life  of  the  patient 
on  the  lines  that  have  been  suggested.  But  in  arterio-sclerosis, 
as  in  other  chronic  diseases,  various  symptoms  may  arise  from 
time  to  time,  and  the  particular  measures  that  are  required 
for  their  relief  are  generally  indicated  by  the  special  disorder. 

It  has  been  urged  that  an  elevated  blood-pressm-e  requires 
reduction,  and  a  host  of  vasodilators  have  been  recommended 
for  this  purpose.  But  in  arterio-sclerosis  the  high  blood- 
pressure  is  really  a  conservative  process,  an  attempt  to  remedy 
circulatory  difficulties  that  have  arisen,  and  any  interference 
with  it  is  just  as  likely  to  do  harm  as  good.  It  is  true  that  in 
the  presence  of  symptoms  the  pressure  may  be  temporarily 
high  for  the  particular  case,  and  with  improvement  often 
falls,  but  in  other  cases  it  rises ;  and  in  the  absence  of  symptoms 
it  is  always  above  normal.  It  is  not  rational  to  conclude  that, 
because  the  blood-pressure  sometimes  falls  coincidently  with 
improvement,  improvement  will  occur  whenever  and  however 
the  pressure  is  lowered.  In  many  cases  this  can  only  be  done 
by  depressing  the  cardiac  action — ^in  short,  by  inducing  cardiac 
failure. 

It  must,  however,  be  admitted  that  practical  experience  has 
shown  that  in  certain  cases  vasodilator  drugs  may  be  of  service. 
In  angina  pectoris,  for  example,  the  inhalation  of  amyl  nitrite 
is  often  of  great  value  during  the  paroxysm,  as  well  as  the 
administration  of  nitro-glycerin  in  the  intervals  between 
attacks.  But  the  action  of  all  drugs  of  this  kind  is  very  fleet- 
ing, erythrol  tetranitrate,  which  is  said  to  have  the  most  pro- 
longed action,  losing  its  effect  within  five  or  six  hours  after  its 
administration;  and  I  have  so  far  failed  to  find  that  their 
continued  use  has  had  any  appreciable  effect  upon  the  blood- 
pressure  curves. 

It  is  somewhat  difficult  to  understand  the  high  reputation 


THE  TREATMENT  OF  ARTERIO-SCLEROSIS       97 

of  iodine  and  the  iodides  in  this  disease,  for  it  seems  certain 
that  they  exercise  Httie  or  no  influence  upon  the  blood-pressure, 
and  their  action  upon  fibrous  tissue  is  only  likely  to  be  effective 
when  it  is  of  syphilitic  origin.  The  general  conclusion  as  to 
their  good  effect  is,  however,  too  strong  to  be  hghtly  dis- 
regarded, and  moderate  doses  may  be  given.  Care  should  be 
taken,  however,  that  iodism  does  not  occur. 

Mercury  is  another  drug  which  has  a  well-established  repu- 
tation in  this  disease,  from  its  action  in  increasing  renal  and 
intestinal  excretion,  and  in  limiting  bacterial  processes  in  the 
intestine.  Calomel  and  blue  pill  seem  to  be  the  most  useful 
preparations.  The  toilet  of  the  mouth  must  be  carefully 
supervised,  particularly  in  those  cases  in  which  renal  symp- 
toms are  prominent. 

In  patients  who  are  more  or  less  convalescent,  these  drugs 
should  be  given  intermittently  rather  than  continuously,  and 
their  effects  are  probably  best  marked  if  they  are  given  every 
alternate  week  or  fortnight,  with  occasional  longer  intervals 
of  intermission. 


CHAPTER  VI 
THE  MYOGENIC  THEORY 

The  cardiac  muscle  differs  morphologically  from  voluntary 
and  involuntary  muscle  elsewhere,  and  the  anatomical  differ- 
ences are  associated  with  differences  in  physiological  action. 
Stimulation  of  voluntary  muscle,  for  example,  is  followed,  after 
the  latent  period,  by  contraction  of  the  muscle,  and  this  in 
turn  by  relaxation;  and  the  cardiac  muscle  also  responds  to 
similar  stimuli,  whether  mechanical,  chemical,  thermal,  or 
electric ;  but  there  are  fundamental  differences  in  the  response. 
During  a  contraction  the  heart  is  refiactory  to  stimuli,  and  a 
tetanus  cannot,  in  consequence,  be  produced.  With  voluntary 
muscle  the  degree  of  contraction  in  response  to  stimulation 
varies  in  direct  accordance  with  the  intensity  of  the  stimulus, 
a  strong  stimulus  producing  a  large  contraction,  and  vice  versa  ; 
but  the  cardiac  muscle  reacts  to  all  stimuli,  whether  great  or 
small,  in  exactly  the  same  way.  During  systole  its  powder 
of  contraction  is  lost,  and  immediately  afterwards  is  at  a 
minimum;  during  diastole  it  rapidly  recovers,  and  a  contrac- 
tion excited  artificially  towards  the  end  of  diastole  is  greater 
than  one  produced  in  the  earlier  periods ;  but  this  is  quite  in- 
dependent of  the  degree  of  stimulation,  the  muscle,  if  excitable, 
reacting  as  strongly  to  a  weak  stimulus  as  to  a  strong  one, 
the  "all  or  nothing  "  motto  of  the  heart.  And,  lastly,  the 
heart  beats  regularly  and  rhythmically  during  hfe,  while^ 
voluntary  muscle  is  inactive  for  long  periods  of  time. 

The  current  theory  of  the  cardiac  action  is  in  some  respects 
a  revival  of  an  old  idea.  It  was  at  first  supposed  that  the 
contractions  were  due  to  the  direct  action  of  the  blood  as  it 
flowed  into  the  auricle,  and  followed  as  soon  as  the  chambers 
were  sufficiently  distended;  but  it  was  soon  shown  that  this. 

98 


THE  MYOGENIC  THEORY  99 

could  not  be  the  case,  as  the  frog's  heart,  when  separated  from 
the  body  and  empty  of  blood,  would  beat  rhythmically  for  a 
considerable  time  if  it  was  placed  under  favourable  conditions 
of  moisture  and  warmth,  so  that  its  rhythmic  action  must  be 
due  to  an  inherent  property  of  the  myocardium.  The  dis- 
covery of  nerve  cells  and  fibres  in  the  heart  then  followed,  and, 
as  respiration  was  at  the  time  considered  to  be  due  to  the 
automatic  action  of  nerve  cells,  the  cardiac  contractions  were 
ascribed  to  a  similar  cause.  The  earlier  theory  was,  however, 
reverted  to  when  Gaskell  showed  that  the  isolated  apex  of  the 
heart,  which  is  devoid  of  nerve  cells,  may  contract  rhythmically 
for  long  periods,  so  that  the  cardiac  beat  must  be  due  to  an 
inherent  power  of  the  muscle  to  produce  rhythmic  stimuH. 

The  wave  of  contraction  starts  at  the  great  veins  and  travels 
through  auricle  to  ventricle,  and  a  controversy  arose  as  to 
whether  the  stimulus  was  conducted  by  nerve  or  by  muscle. 
But  Gaskell  showed  that  in  the  tortoise,  at  any  rate,  the  route 
must  be  muscular,  for  the  coronary  nerve,  the  sole  nervous 
connection  between  auricle  and  ventricle  in  this  animal,  lies 
outside  the  heart  and  can  be  severed  without  disturbing  the 
normal  sequence  of  events ;  while  section  of  the  muscle  alone 
leads  to  asynchronous  contractions  of  the  chambers.  His 
deductions  were  at  first  alleged  to  be  inconclusive  and  in- 
apphcable  to  mammalian  hearts,  as  no  muscular  connection 
between  auricle  and  ventricle  was  known;  but  Stanley  Kent 
and  His  soon  afterwards  demonstrated  the  connecting  fibres, 
the  auriculo-ventricular,  or  a.v.  bundle. 

The  primitive  tissue  of  the  heart  comprises  the  sino-auricular 
node  of  Keith  and  Flack,  the  auriculo-ventricular  node  of 
Tawara,  and  the  auriculo-ventricular  bundle  of  Stanley  Kent. 
The  cells  of  which  these  are  composed  differ  in  some  respects 
from  the  muscle  cells  elsewhere,  being  fusiform  in  shape 
rather  than  rhomboidal,  and  showing  striation  only  at  the 
periphery  of  the  cells.  They  interlace  with  each  other,  and 
possess  a  rather  lar[;G  ovoid  nucleus,  and  are  surrounded  by 
connective  tissue  which  is  somewhat  dense  in  the  sino-auricular 
node,  and  more  clehcate  in  the  auriculo-ventricular  node. 
They  have  a  well-developed  vascular  supply,  and  are  accom- 
panied in  the  sino-auricular  node  by  many  nerve  fibres  and 


100 


DISEASES  OF  THE  HEART 


ganglion  cells  (Fig.  58),  which  are  directly  connected  with  the 
vagus  and  sympathetic  nerves.  The  auriculo-ventricular  node 
contains  nerve  fibres,  but  no  ganghon  cells. 


Fig.  55. — Heart  of  Ox,  dissected  to  show  the  a. v.  Btjxdle  feom  the  Right 
Side  of  the  Heakt.     (A.  Keith.) 


The  sino-auricular  node  is  situated  at  the  junction  of  the 
superior  vena  cava  and  the  right  auricular  appendix  immedi- 
ately beneath  the  epicardium.     It  measures  about  2  mm.  in 


THE  MYOGENIC  THEORY 


101 


thickness,  and  extends  downwards  along  the  sulcus  terminalis 
for  about  2  cm.  The  auriculo-ventricular  node  is  pear-shaped, 
and  measures  about  6  mm.  longitudinally,  and  about  3  mm. 
transverse^.  It  is  situated  (Fig.  56)  on  the  right  side  of  the 
interauricular    septum    close    to    the    anterior   edge  of  the 


Fig.  56. 


-HiTiiAN  Heart,  dissected  to  show  the  a.v.  jSTode  ksd  Bundle 
TEOM  THE  Right  Side  of  the  Heart.     (A.  Keith.) 


coronary  sinus,  and  immediately  above  the  insertion  of  the 
median  cusp  of  the  tricuspid  valve.  The  fibres,  as  they  leave 
the  node,  are  collected  together  into  the  auriculo-ventricular 
bundle  (Figs.  55,  56,  57),  which  passes  forwards  in  the  inter- 
auricular septum,  and  then  turns  abruptly  downwards,  pre- 
forating  the  central  fibrous  body  of  the  heart  to  reach  the 


102 


DISEASES  OF  THE  HEART 


interventricular  septum  immediately  behind  tlie  membranous 
space.  As  it  approaches  the  lower  border  of  the  space,  it 
divides  into  two  main  branches,  which  separate  and  run 
downwards   beneath   the   endocardium   on   each   side   of   the 


Fig.  57. — Heart  of  Waxbus,  dissected  to  show  the  a. v.  Bundle  from  the 
Left  Side  of  the  Heart.     (A.  Keith.) 


septum.  The  branches,  as  they  descend,  spread  out  fanwise, 
and  apparently  end  in  the  muscle  cells  which  clothe  the  in- 
terior of  the  ventricles,  the  papillary  muscles  in  particular 
receiving  an  ample  supply. 

The  cells  of  the  system  vary  somewhat  in  size  in  the  lower 


THE  MYOGENIC  THEORY 


103 


animals,  the  Purkinje  fibres  being  tbe  largest  and  those  in  the 
nodes  the  smallest.  The  cells  of  the  auriculo-ventricular  node 
and  bundle  are  in  direct  connection  with  each  other,  but  those 
of  the  sino-auricular  and  auriculo-ventricular  nodes  have  not 
yet  been  shown  to  be  continuous,  as  their  cells  seem  to  pass 
gradually  into  the  auricular  muscle  and  to  lose  their  special 
characters. 

The  primitive  tissue  of  the  heart  is  recognized  to  be  the 
representative  of  the  primitive  tubular  heart  which  is  formed 
by  the  coalescence  of  the 
two  symmetrical  ventral 
tubes  of  the  hsemoccelum. 
In  the  course  of  the 
development  of  the  heart 
saccular  chambers  are 
formed,  which  ultimately 
become  the  auricles  and 
ventricles,  and  these  are 
at  first  separated  from 
each  other  by  the  auri- 
cular canal.  In  the  lower 
vertebrates,  however,  the 
auricular  canal,  owing  to 
the  telescoping  of  auricles 
and  ventricles  upon  each 
other,  is  merely  repre- 
sented by  the  circular 
fibres  at  the  auriculo- 
ventricular  junction, 
though  the  sinus  venosus, 

auricles,  ventricles,  and  bulbus  cordis  are  still  distinct.  In 
the  mammahan  heart  the  distinction  is  still  more  confused, 
for  the  sinus  has  become  lost  in  the  great  veins  and  the  adja- 
cent auricular  tissue,  and  the  bulbus  incorporated  in  the 
infundibulum  of  the  right  ventricle.  The  s.a.  node  is  a  remnant 
of  the  sinus  venosus,  and  the  a.v.  node  and  bundle  are  the  sole 
surviving  cells  of  the  auricular  canal.  The  ceUs  of  the  bulbus 
are  indistinguishable  from  the  ventricular  muscle. 

At  the  present  time  it  is  generally  believed  that  the  rhythmic 


Fig.  58. — The  SiJfo-AuEicuLAR  Node,  show- 
ing Nodal  Tissue  and  Ganglion  Cells. 


104  DISEASES  OF  THE  HEART 

action  of  the  heart  and  the  proper  sequence  of  contraction  of 
the  various  chambers  are  intimately  connected  with  the  in- 
tegrity of  the  primitive  tissue.  The  histological  differences 
between  these  fibres  and  the  rest  of  the  cardiac  muscle  imply 
functions  of  a  different  nature,  and  the  bundle,  at  any 
rate,  has  been  definitely  proved  to  be  concerned  mth  the 
passage  of  the  stimulus  from  auricle  to  ventricle,  for  it  has 
been  shown  repeatedly  that  its  destruction  produces  heart- 
block. 

In  the  course  of  development  specialization  of  function  has 
occurred.  In  the  primitive  heart  rhj'thmicity  and  contractile 
power  are  fairty  equally-  developed,  and  a  contraction  can 
originate  in  any  part  of  its  length.  But  in  the  vertebrate 
heart  the  auricles  and  ventricles  have  developed  their  con- 
tractile power,  and  lost  to  some  extent  their  power  of  originat- 
ing contractions,  and  they  only  respond  with  an  isolated  beat 
to  a  single  (experimental)  stimulus.  The  parts,  however, 
which  remain  least  altered — the  sinus,  the  a.v.  tissues,  and  the 
bulb — have,  however,  in  the  frog  a  rhythmic  power  which  is 
greatty  in  excess  of  that  of  auricle  and  ventricle,  and  readily 
initiate  contractions  spontaneously,  and  respond  in  answer  to 
minimal  stimuli,  not  with  an  isolated  contraction,  but  with  a 
series  of  beats.  The  normal  contraction  of  the  auricle  starts 
in  the  vicinity  of  the  s.a.  node,  and  an  extra-systole  produced 
experimentally  by  stimulation  of  this  area  gives  an  electrical 
response  precisely  similar  to  that  of  the  normal  beat,  so  that 
the  normal  auricular  stimuli  presumably  arise  in  this  situa- 
tion. The  response,  however,  is  universal,  all  the  cardiac 
muscle  contracting  in  sequence,  a  sequence  which  is  regular  in 
cases  where  the  a.v.  bundle  is  intact.  If  the  latter,  however, 
is  functionally  inactive,  the  regular  sequence  is  interrupted, 
and  the  auricles  and  ventricles,  if  they  contract  at  all,  do  so 
irrespective  of  each  other,  and  at  a  totally  different  rate,  the 
auricular  contractions  numbering  about  seventy  and  the  ven- 
tricular contractions  about  thirty  per  minute. 

The  ventricular  contractions  in  this  case  are  not  in  response 
to  the  normal  sinus  stimuli,  but  in  answer  to  stimuh  which 
arise  in  the  ventricular  substance;  and  James  Mackenzie  has 
suggested  that  the^^  may  arise  in  that  part  of  the  primitive 


THE  MYOGENIC  THEORY  105 

tissue — the  terminal  branches  of  the  a.v.  bundle — which  are 
present  in  the  ventricles.  In  full  heart-block  the  rhythm  of 
the  ventricles  may  be  quite  regular,  a  fact  which  suggests  that 
the  stimuli  habitually  arise  in  the  same  situation;  and  electro- 
cardiograms show  a  normal  ventricular  complex,  so  that  the 
contractions  originate  in  the  vicinity  of  the  auriculo-ventricular 
junction  in  the  region  where  the  a.v.  bundle  is  situated.  The 
theory  is  attractive,  but  the  evidence  in  its  favour,  though 
suggestive,  is  not  yet  conclusive.  It  must,  too,  be  remem- 
bered that  the  cardiac  contraction  starts  in  the  great  veins, 
and  not  in  the  auricles.  The  nodes  may  be  the  "clearing- 
house," rather  than  the  head  office  of  the  bank. 

The  influence  of  the  nervous  system  upon  the  heart  is  very 
apparent  both  in  experiment  and  in  the  clinique,  but  it  is 
regulative  rather  than  essential,  for  the  isolated  heart  can  con- 
tract regularly  for  considerable  periods  under  favourable  con- 
ditions. All  the  functions  of  the  heart — stimulus  production, 
excitability,  contractility,  conductivit}-,  and  tonicity — may  be 
affected,  but  our  present  knowledge  is  as  yet  insufficient  to 
enable  us  to  determine,  unless  in  very  exceptional  instances, 
whether  functional  disturbances  of  the  cardiac  action  are  due 
to  intrinsic  or  to  extrinsic  causes.  Both  may  be  in  action  at 
the  same  time,  or  one  or  other  alone,  and  it  seems  probable 
that  in  the  former  case  the  actions  of  the  two  are  sometimes 
antagonistic,  the  one  endeavouring  to  minimize  or  to  prevent 
a  detrimental  activity  of  the  other.  The  present  position  is 
thus  too  indefinite  for  useful  discussion,  but  it  may  be  stated 
that  the  available  evidence  suggests  that  exactly  similar  dis- 
turbances may  be  produced  by  either  cause,  or  at  any  rate 
may  be  due  to  causes  originating  without  the  heart  as  well  as 
within  it. 

The  investigation  of  the  special  functions  of  the  cardiac 
muscle,  its  power  of  producing  rhythmic  stimuli,  its  excita- 
bihty  and  contractihty,  the  variations  in  the  rate  of  conduc- 
tion of  the  stimuli  from  part  to  part,  and  the  tonicity  of  the 
organ  as  a  whole,  has  been  pursued  in  the  laboratory'  for  many 
years  past;  but  it  has  only  been  possible  within  the  last  few 
years  to  apply  laboratory  methods  to  chnical  work,  and  to 


106  DISEASES  OF  THE  HEART 

investigate  tlie  different  functions  individually.  By  graphic 
methods  the  relationship  of  the  contractions  of  the  various 
chambers  can  be  readily  demonstrated,  and  the  advance  in 
our  knowledge  of  cardiac  disease  has  been,  in  consequence, 
considerable.  Much  work  has  been  done,  and  some  problems 
have  already  been  solved,  but  many  more  await  solution. 
Some  of  the  current  theories  may  be  disproved  in  course  of 
time,  and  others  may  be  verified,  but  the  newer  methods  have 
added  greatly  to  precision  in  diagnosis,  prognosis,  and  treat- 
ment; and  a  proper  conception  of  the  processes  which  have 
produced  cardiac  failure  in  the  individual  case  can  only  be 
attained  by  appreciation  of  the  character  and  the  site  of  the 
special  disturbance. 


la        I     -75       I       a       I      -8        I        B        I      7^-1        a        I      ^♦-^-^ 


Fig.  59. — Brachial,  Cervxcal,  ksb  Apex  Curves,  showing  the  Relationship 
OF  THE  Various  Waves. 

1,  Commencement  of  auricular  wave  on  apex  tracing;  2,  commencement  of  ven- 
tricular upstroke  on  apex  tracing;  3,  appearance  of  carotid  wave  in  cervical 
curve;  4,  appearance  of  brachial  wave;  5,  termination  of  ventricular  plateau 
on  apex  tracing;  6,  termination  of  ventricular  wave  on  apex  tracing. 


The  Interpretation  of  Polygraph  Curves. — ^The  interpretation 
of  the  cervical  curves  requires  detailed  consideration,  for  it 
must  be  remembered  that  the  causes  producing  the  variations 
in  pressiKe  within  the  cavities  of  the  heart,  as  shown  experi- 
mentally, are  not  yet  accurately  known,  while  the  data  avail- 
able in  chnical  work  are  even  less  numerous  and  more  obscure. 
The  main  points,  however,  can  be  seen  on  examination  of 
Figs.  59  and  60.  In  both  figures  the  upper  curve  is  from  the 
brachial  artery  at  the  level  of  the  elbow;  the  central  curve  is 
from  the  right  neck  immediately  above  the  clavicle,  and  just 
outside  the  sterno-mastoid  muscle;  while  the  lowest  curve  is 


THE  MYOGENIC  THEORY 


107 


from  tlie  apex  impulse.  The  curves  are  thus  not  strictly  com- 
parable, for  while  the  first  two  are  records  of  changes  in  the 
volume  (mainly)  and  the  pressure  within  the  vessels,  the  third 
is  the  record  of  the  varying  relationship  of  the  apex  impulse 
to  the  chest  wall,  and  not  of  the  intraventricular  pressure. 

The  apex  tracings  show  as  a  rule  one  well-sustained  wave 
and  several  smaller  ones,  the  large  wave  representing  the 
ventricular  systole.  Three  phases  of  the  latter  can  be  recog- 
nized :  the  more  or  less  abrupt  but  inclined  line  of  ascent,  the 
flat-topped  plateau  of  the  summit,  which  may  be  broken  up 
into  several  minor  waves,  and  the  gradual  fall  to  the  base-line. 
During  the  first  phase  the  intraventricular  pressure  is  rising 
until  it  becomes  greater  than  the  pressure  within  the  great 
arteries,  when  the  valves  open  and  blood  commences  to  flow 
out  of  the  heart.     The  exact  time  of  this  occurrence  is  not 


Fig.  60. — Brachial,  Cervical,  ajs^d  Apex  Ctjeves,  showing  Absence  of 
X  Negative  Wave. 


precisely  indicated  on  the  curve,  and,  indeed,  is  variable  in 
different  cases  (presphygmic  interval,  0'02  to  0*085  second 
Lewis;  cf.  Fig.  61),  from  variations  in  the  aortic  pressm'e  at 
the  end  of  diastole  and  in  the  relative  strength  of  the  ven- 
tricular systole.  During  the  period  covered  by  the  plateau 
the  output  is  maintained,  and  about  its  termination  diastole 
commences  and  the  semilunar  cusps  close.  With  relaxation 
of  the  ventricle  the  curve  rapidly  falls,  and  as  soon  as  the 
pressure  within  the  auricle  exceeds  the  pressure  within  the 
ventricle,  the  auriculo-ventricular  valves  open — a  time  which 
coincides  fairly  accuratelj^  with  the  lowest  point  upon  the 
tracing.  Succeeding  the  fall  there  is  often  a  well-marked  wave 
— an  instrumental  fault  due  to  the  momentum  of  the  recording 
lever,  and  best  marked  in  cases  where  the  fall  is  most  abrupt. 
As  diastole  proceeds,  the  curve  gradually  rises  as  the  ventricle 


108  DISEASES  OF  THE  HEART 

again  becomes  distended  with  blood.  Towards  the  end  of 
ventricular  diastole  the  small  wave  a  is  seen,  the  result  of  the 
contraction  of  the  auricle.  The  a  wave  is  not  invariably 
present  in  the  tracing,  and  may  be  absent  in  cases  where  other 
evidence  of  auricular  activity  is  undoubtedly  present. 

The  rise  in  the  brachial  curve  is  distinctly  later  than  the 
commencement  of  the  ventricular  wave  on  the  apex  tracing, 
the  delay  being  due  to  the  presphygmic  interval,  and  to  the 
time  occupied  in  the  transmission  of  the  pulse  wave  from  the 
aorta  to  the  brachial  artery  {cf.  Fig.  61) — a  period  which  neces- 
sarily varies  according  to  the  distance  between  the  two  points. 

The  cervical  curve  shows  a  variable  number  of  waves,  which 
are  due  to  various  causes.     The  receiver  of  the  polygraph  is 


<3,^>vto  J)  ^y-«-   '*- 


Fig.  61. — Brachial  and  Apex  Curves,  and  Tracing  (Centre)  from  Second 
Left  Intercostal  Space  Close  to  the  Sternum. 

The  wave  P  is  evidently  derived  from  the  pulmonary  artery,  and  succeeds  the 
rise  of  the  ventricular  wave  on  the  apex  tracing.  The  interval  between 
these  events  is  the  presphygmic  interval. 

placed  (Fig.  62)  immediately  over  the  carotid  arter}'  and  the 
jugular  vein,  and  the  resultant  tracing  is  a  complex  of  the 
variations  in  volume  and  in  pressure  which  are  occiirring  in 
these  vessels. 

The  essential  point  in  the  interpretation  of  the  curve  is  the 
detection  of  the  carotid  wave  c  (3),  which  makes  its  appear- 
ance shortly  after  the  commencement  of  the  ventricular  con- 
traction (2),  as  shown  on  the  apex  tracing,  and  shortly  before 
the  appearance  of  the  pulse  in  the  brachial  artery  (4),  and  c 
may  be  identified  by  reference  to  either.  If  there  is  any  doubt, 
the  receiver  may  be  moved  slightly  higher  up  the  neck  above 
the  valves  in  the  jugular  vein,  and  a  pure  carotid  tracing 
obtained  for  comparison.  There  has  been  some  discussion  as 
to  the  precise  significance  of  the  c  wave,  for  a  wave  has  been 


THE  MYOGENIC  THEORY 


109 


recorded  at  practically  the  same  time  in  tracings  of  intra- 
auricular  pressm^e,  as  well  as  in  animals  whose  jugular  vein 
has  been  dissected  out  free  from  all  Connection  with  the  carotid 
artery,  so  that  it  must  be  admitted  to  be  possibly  due  to  causes 
operating  in  the  jugular  bulb.  The  wave  in  question  arises 
during  the  period  of  ventricular  systole,  and  is  probably  due 
to  ballooning  upwards  of  the  auriculo-ventricular  valve  during 


:Sterno  mastoid 
i 


^i-O 


Clavicle 


Manubrium  sterni 


Fig.  62. — Diagram  showing  the  Situation  of  the  Carotid  Artery  and  the 
JuGUi/AR  Vein.     (A.  Keith.) 

The  circle  shows  the  position  of  the  receiver  of  the  polygraph. 


that  event;  but  it  is  not  invariably  present  in  all  tracings  of 
intra-auricular  pressure,  and  it  is  usually  small.  Firm  pres- 
sure of  the  receiver  in  the  neck  frequently  produces  a  wave  of 
typical  arterial  form,  and — in  the  vast  majority  of  cases,  at 
any  rate — the  c  wave  is  due  to  the  carotid  pulse. 

Immediately  preceding  c  is  the  wave  a.  It  occurs  about 
0*15  to  0"20  second  before  c,  and  synchronously  with,  or  im- 
mediately after,  the  a  wave  on  the  apex  tracing,  and  is  the 


110  DISEASES  OF  THE  HEART 

result  of  auricular  contraction.  There  is  but  little  delay  in 
its  appearance,  for  there  are  no  valves  between  the  auricle  and 
the  jugular  bulb  beneath  the  receiver,  and  the  distance  is  but 
short ;  so  that  variations  in  pressure  within  the  auricle  are 
rapidly  transmitted  to  the  jugular  vein.  There  is  still  some 
doubt  as  to  its  exact  significance,  and  it  has  been  ascribed  to 
regurgitation  into  the  veins  during  auricular  systole,  and  to 
stasis  in  the  veins  without  regurgitation,  following  the  sudden 
rise  of  auricular  pressure  during  systole.  From  a  practical 
point  of  view  the  distinction  is  immaterial,  and  the  wave  may 
be  considered  as  definite  evidence  of  auricular  contraction. 

The  wave  v  following  c  varies  considerably  in  different  cases, 
both  in  the  time  of  its  occurrence  and  in  its  form.  In  many 
cases  it  is  separated  from  c  b}-  the  negative  depression  x,  and 
it  may  be  single  or  double  (wi-Vg). 

The  early  part  at  any  rate  occurs  during  ventricular  systole, 
and  the  notch  between  the  two  peaks  of  the  double  wave  is 
generally  synchronous  with  the  termination  of  the  systohc 
plateau  (5)  in  the  apex  tracing.  With  the  onset  of  ventricular 
systole  the  auriculo-ventricular  valve  is  closed,  and  the  pres- 
sure within  the  auricle  is  at  its  minimum.  During  ventricular 
systole  venous  blood  gradually  enters  the  auricle,  and  the 
pressure  within  it  rises  steadily  until  at  the  completion  of 
ventricular  systole  the  auriculo-ventricular  valves  again  open, 
and  the  auricular  pressure  falls  as  the  blood  flows  from  the 
auricle  into  the  ventricle,  and  the  wave  in  consequence  dies 
away. 

The  second  wave  V2,  however,  occurs  after  the  systolic 
plateau  has  ended,  and  is  therefore  ventricular  diastohc  in 
time,  and  its  occurrence  must  be  due  to  other  causes. 

During  the  contraction  of  the  heart  the  apex  is  the  only 
part  which  remains  constant  in  position  within  the  chest- 
During  auricular  systole  the  auriculo-ventricular  junction  is 
pulled  upwards  towards  the  great  veins,  and  during  ventricular 
systole  pulled  downwards  towards  the  apex  (Keith),  and  the 
ventricular  movement  downwards  expanding  the  auricle  is 
probably  the  chief  cause  of  the  negative  depression  or  wave  x. 
When  ventricular  systole  ceases,  the  pull  on  the  auriculo- 
ventricular   junction   ceases,    too,    and   it   resumes   its    mean 


THE  MYOGENIC  THEORY  111 

position,  and  the  "rebound,"  when  it  is  active,  produces  the 
positive  variation,  wave  v<i,  in  the  jugular  curve. 

In  certain  cases  v  vnsbj  occur  earlier  in  the  tracing,  and  it 
may  even  merge  into  c,  as  in  Fig.  60.  This  may  be  due  to  two 
causes :  v  will  appear  the  earlier  the  more  rapid  the  diastohc 
filling  of  the  auricle,  and  this  will  obtain  whenever  there  is 
venous  engorgement ;  and  it  will  also  occur  early  if  the  auriculo- 
ventricular  valve  is  incompetent,  and  blood  regurgitates  into 
the  auricle  at  the  commencement  of  ventricular  systole. 

The  depression  x  has  alreadj^  been  ascribed — in  part,  at  any 
rate — ^to  the  negative  pressure  produced  in  the  auricle  during 
ventricular  systole  by  the  displacement  of  the  auriculo-ven- 
tricular  junction.  Another  factor  probably  coexists.  During 
ventricular  systole  blood  is  forced  out  of  the  chest  into  the 
arteries,  and  the  intrapleural  pressure  falls  as  a  result,  and  the 
intra-auricular  pressure  will  foUow  suit. 

The  depression  y  (Fig.  59),  which  foUows  v,  is  the  result  of 
ventricular  diastole.  As  soon  as  the  auriculo-ventricular 
valves  open,  blood  flows  from  auricle  to  ventricle,  and  the 
auricular  and  the  jugular  pressures  fall  until,  with  the  lapse  of 
time,  both  auricle  and  ventricle  are  again  filled  by  the  inflow 
of  the  venous  blood,  and,  in  consequence,  the  lever  gradually 
rises  during  diastole. 

There  has  been  much  difference  of  opinion  as  to  the  precise 
time  of  the  closure  of  the  semilunar  valves  and  the  opening  of 
the  auriculo-ventricular  valves. 

It  seems  quite  certain  that  the  time  of  the  opening  and  the 
closure  of  the  semilunar  valves  cannot  be  recognized  upon  the 
apex  tracing.  The  valves  open  synchronously  with  the  ap- 
pearance of  the  aortic  pulse,  and  close  coincidently  with  the 
occurrence  of  the  dicrotic  notch,  and  experimental  curves  show 
that  these  events  have  no  constant  relationship  with  the  apex 
tracing,  varying  considerably  in  different  cases,  the  opening 
occurring  during  the  fine  of  ascent,  and  the  closure  before, 
at,  or  after  the  termination  of  the  plateau.  The  trans- 
mission time,  too,  varies,  and  corresponding  periods  in  the 
carotid  or  brachial  pulse  cannot  be  accurately  related  to  the 
same  events  in  the  aorta. 


112  DISEASES  OF  THE  HEART 

A  similar  conclusion  must  be  asserted  with  regard  to  the 
period  when  the  auriculo-ventricular  valves  open.  It  seems 
certain  that  they  close  synchronously  with  the  commencement 
of  the  upstroke  of  the  sj^stoHc  plateau,  and  that  the}^  open 
after  ventricular  systole  has  ceased,  as  soon  as  ventricular 
relaxation  has  reduced  the  intraventricular  pressure  below 
that  in  the  auricle ;  but  the  pressure  within  the  auricle,  at  the 
commencement  of  ventricular  diastole,  maj^  var}^  even  in  the 
same  case  from  varying  degrees  of  engorgement  of  the  veins, 
varying  length  of  ventricular  systole,  etc.,  and  the  rapidity  of 
lowering  of  ventricular  pressure  is  also  inconstant,  so  that  the 
relationship  on  the  apex  tracing  cannot  be  fixed.  The  cervical 
curve  is,  however,  a  more  accurate  guide,  and  the  apex  of  v 
(or  the  notch  between  v^  and  Vg)  seems  probabty  the  period 
required. 

The  a-c  interval  in  the  cervical  curve  has  acquired  con- 
siderable importance,  since  it  is  used  as  an  index  of  the  time 
occupied  b}^  the  transmission  of  the  stimulus  from  auricle  to- 
ventricle.  In  a  general  way  the  deduction  is  justified,  but  it 
must  not  be  carried  too  far.  During  the  a-c  interval  five 
events  occur:  (1)  The  contraction  of  the  auricle;  (2)  the  pas- 
sage of  the  stimulus  from  auricle  to  ventricle;  (3)  the  latent 
period  after  the  stimulus  has  reached  the  ventricle;  (4)  the 
presphygmic  interval;  and  (5)  the  time  occupied  by  the  trans- 
mission of  the  pulse  wave  from  aorta  to  carotid.  The  a  wave 
is  not  an  accurate  index  of  the  duration  of  auricular  systole, 
for  experimental  evidence  points  to  the  continuance  of  auricular 
contraction  after  ventricular  contraction  has  commenced.  We 
have  no  knowledge  of  the  duration  of  the  latent  period,  but 
we  know  that  the  presphygmic  interval  varies  considerably 
(0"02  to  0'085  second)  in  experimental  curves,  and  that  the 
transmission  time  depends  upon  the  distance  traversed,  the 
aortic  pressure  at  the  end  of  diastole,  and  the  pressure  reached 
during  the  presphygmic  interval.  Chnically,  the  two  items  can- 
not be  separated,  but  together  (commencement  of  V  in  apex 
tracing — appearance  of  c  in  cervical  curve)  they  may  vary  from 
0-03  to  0*11  second. 

The  a-c  interval  measures  as  a  rule  0'  15  to  0-20  second,  and 
it  is  not  likely  to  be  greatly  prolonged  by  variations  in  factors 


THE  MYOGENIC  THEORY  113 

1,  3,  4,  5.  If  it  exceeds  0-25  second,  conduction  is  probably 
defective  and  prolonged,  but  smaller  variations  from  tlie 
average  may  perhaps  be  produced  by  other  causes. 

H  (b)  Wave. — In  slowly  beating  hearts  a  wave  {h  or  h)  may 
be  seen  in  the  cervical  curves  between  v  and  the  succeeding 
a  waves  (Fig.  63).  Its  time  relationship  to  the  preceding 
c  wave  is  constant  in  the  particular  case  (about  0*  50  second), 
and  it  has  been  ascribed  by  A.  G.  Gibson  and  Hirschfelder  to 


EiG.  63. — Ceevical  a^-d  Apex  Ctteves,  showing  the  Wave  Ti  or  h. 

the  snapping  together  of  the  cusps  of  the  aiu'iculo-ventricular 
valve  at  the  end  of  ventricular  filling  in  micl-diastole.  A 
similar  wave  may  be  present  in  oesophageal  tracings.  When 
the  pulse  quickens,  the  wave  in  question  disappears. 

In  cases  of  lengthened  a-c  interval  the  possibility  of  h  and  a 
being  mingled  together  must  be  borne  in  mind.  The  fallacy 
can  be  detected  by  reference  to  the  apex  tracing,  as  the  com- 
mencement of  a  in  the  cervical  curve  and  a  in  the  apex  tracing 
do  not  coincide. 

REFERENCES. 

G.  A.  Gibson:  The  Nervous  AfEections  of  the  Heart,     Edinburgh,  1904. 
W.  H.  Gaskell:  Article  in  Schafer's  Textbook  of  Physiology,  vol.  ii.     Edin- 
burgh and  London,  1900. 
JoknIIay:  Graphic  Methods  in  Heart  Disease.     London,  1909. 
T.Lewis: 

Article  in  Hill's  Further  Advances  in  Physiology.     London,  1909. 

Mechanism  of  the  Heart-Beat.     London,  1911. 
James  Mackenzie: 

The  Study  of  the  Pulse.     Edinburgh  and  London,  1902. 

Diseases  of  the  Heart.     London,  1908. 
P.  Mkrklen:  Les  Troubles  Functionnels  du  Coeur.     Paris,  1908. 
W.  T.  Ritchie  :  The  Action  of  the  Vagus  on  the  Human  Heart.     Quart.  Journ. 

of  Med.,  1912,  Oxford,  vol.  vi.,  p.  47. 
H.  Vaquez:  Les  Arythmies.  Paris,  1911. 
K.  F.  Wenckebach:  Arhythmia  of  the  Heart.     Edinburgh,  1904. 

8 


CHAPTER  VII 
THE  ELECTRO-CARDIOGRAPH 

By  W.  T.  Ritchie 

When  any  point  of  a  muscle  or  other  excitable  tissue  is 
stimulated,  a  change  of  electric  potential  is  induced.  The  part 
which  is  stimulated  and  in  activity  becomes  electro-negative 
to  the  parts  at  rest,  and  may  be  regarded  as  corresponding  to 
the  zinc  plate  of  a  galvanic  cell;  the  remainder  of  the  muscle, 
which  is  at  rest,  corresponds  to  the  copper  plate.  If  the  active 
and  passive  portions  of  a  muscle  are  connected  by  means  of 
electrodes  to  a  sensitive  galvanometer,  the  changes  in  electric 
potential  accompanying  muscular  activity — the  action  currents 
of  the  muscle — can  be  recorded  by  the  instrument.  Waller, 
in  1887,  was  the  first  to  register  the  action  currents  of  the 
human  heart.  He  employed  a  capillary  electrometer,  and 
showed  that  they  were  transmitted  throughout  the  body,  and 
could  be  led  off  from  moist  skin  surfaces.  But  as  action  cur- 
rents are  extremely  feeble,  and  as  the  interpretation  of  capil- 
lary electrometer  curves  is  attended  with  considerable  diffi- 
culty, Einthoven  employed  the  string  galvanometer,  and  it  is 
this  instrument,  with  his  modifications,  that  is  now  being  used 
extensively  in  physiological  and  chnical  work. 

The  string  galvanometer  is  based  on  the  principle  that  a 
moving  conductor  (a  fijie  fibre),  suspended  in  a  magnetic  field 
at  right  angles  to  the  lines  of  force,  tends  to  be  deflected  to 
one  side  or  other  according  to  the  direction  of  the  current. 
The  extent  to  which  the  fibre  is  deflected  varies  in  direct  pro- 
portion to  the  intensity  of  the  current  passing  through  it,  and 
to  the  strength  of  the  magnetic  field,  and  inversely  to  the 
weight  and  tension  of  the  fibre.  In  Einthoven's  string  gal- 
vanometer the  currents  are  led  through   an    extremely  fine 

114 


THE  ELECTHO-CARDIOGRAPH  115 

silvered  glass  or  quartz  fibre,  which  is  stretched  between  the 
poles  of  a  powerful  electro-magnet.  Accompanying  each  con- 
traction of  the  heart  there  are  changes  of  electric  potential;, 
the  fibre  oscillates  to  and  fro,  and  its  shadow  can  be  projected 
upon  a  moving  photographic  plate.  The  record  thus  obtained 
is  termed  an  "  electro-cardiogram." 

The  records  should  be  taken  while  the  patient  is  recumbent 
or  rechning  quietly  in  a  chair,  so  as  to  avoid  as  far  as  possible 
all  tremor  of  the  somatic  muscles,  which  distort  the  electro- 
cardiogram. The  currents  are  led  off  from  the  two  hands,  or 
from  one  hand  and  one  foot,  immersed  in  porous  jars  filled  with 
sahne  solution.  These  jars  He  within  earthenware  pots  con- 
taining zinc  sulphate  solution  and  an  amalgamated  zinc  rod,, 
which  can  be  connected  to  the  ends  of  the  fibre.  The  proce- 
dure is  consequently  not  more  irksome  to  the  patient  than 
that  entailed  in  obtaining  a  graphic  record  by  means  of  the 
polygraph.  As  compared  with  the  polygraph,  the  string  gal- 
vanometer has  the  great  advantage  of  ehminating  the  fallacies 
dependent  upon  inertia,  and  upon  the  delay  in  the  transmis- 
sion of  mechanical  impulses.  Its  chief  value,  however,  con- 
sists in  the  fact  that  by  it  alone  do  we  obtain  information 
regarding  the  essential  nature  of  each  heart-beat. 

The  form  of  the  electro-cardiogram  varies  according  to  the 
derivation  that  is  employed.  Follo\\dng  Einthoven's  nomen- 
clature, a  lead  from  the  right  hand  and  left  hand  is  termed 
"Derivation  /.,"  that  from  the  right  hand  and  left  foot  is 
''Derivation  //.,"  and  that  from  the  left  hand  and  left  foot 
is  "Derivation  ///."  When  recording  electro-cardiograms  it 
is  customary  to  adopt  Einthoven's  standard,  and  to  a-djust  the 
tension  of  the  fibre  so  that,  -with  a  constant  magnification,  its 
shadow  is  deflected  1  cm.  when  a  difference  of  potential  of 
1  milhvolt  is  introduced  into  the  circuit  containing  the  gal- 
vanometer and  the  patient.  It  is,  therefore,  possible  to  insti- 
tute a  comparison  of  the  amphtude  of  the  individual  deflexions 
in  different  records. 

Fig.  64  shows  a  normal  electro-cardiogram  by  Derivation  II, 
Each  upward  deflexion  P,  R,  and  T,  indicates  that  either  the 
base  or  right  side  of  the  heart  was  electro-negative,  and  there- 
fore in  predominant  activity,  whereas  the  downward  deflexions 


116  DISEASES  OF  THE  HEART 

Q  and  &  signify  negativity — ^.e.,  predominant  activity — of  the 
apex  or  left  side  of  the  heart.  P  is  the  auricular  deflexion; 
Q,  R,  S,  and  T  are  ventricular  deflexions.  In  some  instances 
T  is  succeeded  by  another  upward  deflexion,  U.  Fig.  65 
demonstrates  the  time  relation  of  the  waves  in  the  cervical 
cm've  to  the  electro-cardiographic  deflexions.  The  auricular 
wave,  a,  in  the  jugulo-carotid  tracing  is  later  than  the  electro- 
cardiographic deflexion  P,  owing  to  the  material  delay  in  the 
transmission  of  impulses  recorded  by  the  potygraph.  The 
carotid  wave,  c,  is  later  than  the  deflexion  R  for  the  same 
reason,  and  also  because  of  the  presphygmic  period  and  the 
delay  in  the  transmission  of  the  pulse  wave  from  the  aortic 
valve  to  the  carotid  artery. 

The  Electro-Cardiographic  Deflexions. — In  a  healthy  heart  the 
auricular  deflexion,  P,  is  a  simple  upward  deflexion.     Although 


Fig.  64. — ^Normal  Electeo-Cabdiogkam. 
Derivation  II.  1  mi]livolt=l  cm.     Time  record  is  28'o  per  second. 

the  amphtude  of  the  electro-cardiographic  deflexions  cannot  be 
regarded  as  a  definite  measure  of  the  electro-motive  force  of 
the  heart,  we  nevertheless  find  that  P  is  larger  than  normal  in 
cases  of  auricular  hypertrophy,  and  more  especially  in  cases 
of  mitral  stenosis.  When  P  is  of  abnormal  form — diphasic, 
inverted,  etc. — it  is  generally  supposed  that  the  auricular  con- 
traction has  started  at  some  other  site  than  the  normal  one  in 
the  sino-auricular  node.  For  example,  diphasic  auricular  de- 
flexions may  ensue  when  the  heart  is  retarded  by  stimulation 
of  the  vagus,  or  when  the  auricles  are  in  flutter  (Fig.  70). 
According  to  Rothberger  and  Winterberg,  P  becomes  inverted 
when  the  left  accelerator  nerve  is  stimulated,  and  it  is  prob- 
able that  under  these  circumstances  the  left  auricle  begins  to 
contract  before  the  right. 


THE  ELECTRO-CARDIOGRAPH  117 

During  the  interval  between  P  and  Q,  while  the  curve 
remains  horizontal,  the  ventricles  are  still  at  rest ;  and  although 
a  stimulus  is  passing  along  the  auriculo-ventricular  system  to 
the  ventricles,  the  accompanying  change  of  potential  is  too 
weak  to  cause  any  deflexion  of  the  fibre. 

Q,  B,  S,  and  T  are  the  deflexions  resulting  from  ventricular 
activity.  Their  precise  interpretation  is  still  a  matter  of 
doubt  and  discussion.  The  deflexions  Q,  R,  and  S  probably 
indicate  that  the  stimulus  passing  from  the  auricles  along  the 
terminal  ramifications  of  the  a.v.  bundle  reaches  different  parts 
of  the  ventricles  ahnost  simultaneously.  E  is  the  most  con- 
stant of  all  the  deflexions,  and  is  generally  regarded  as  signi- 


Fig.  65. — Simultaneous  Records  of  the  CER\acAL  Curve  axd  of  the  Electro- 
Cardiogram  (Derivation  //.).  illustrating  the  Time  Relation  of  the 
Waves  in  the  Cervical  Curve  and  the  Deflexions  of  the  Electro- 
Cardiogram. 

P  precedes  a,  and  R  precedes  c. 

fying  contraction  of  the  basal  part  of  the  papillary  muscle 
system.  The  fijst  sound  commences  0'02  to  0"03  second  after 
the  beginning  of  the  first  ventricular  deflexion.  The  period 
between  S  and  T,  during  which  the  line  of  the  curve  is  again 
horizontal,  coincides  with  the  contraction  of  the  main  mass  of 
ventricular  muscle.  The  action  currents  compensate  one 
another  meanwhile,  so  that  there  is  no  predominance  of  activity 
either  at  base  or  apex  or  of  one  ventricle  over  the  other.  In 
the  case  of  a  healthy  heart,  the  final  deflexion,  T,  is  upwards. 
Some  authorities  regard  an  upward  T  as  signifying  that  the 
right  ventricle  remains  in  contraction  longer  than  does  the 
left,  whereas  others  conclude  that  when  each  contraction  wave 


118 


DISEASES  OF  THE  HEART 


spreads  through  the  ventricular  muscle  the  last  portion  to  con- 
tract is  that  near  the  aorta  and  pulmonary  artery.  Jolly  and 
the  writer  have  concluded  that  in  records  by  Derivation  I. 
an  upward  T  may  be  regarded  as  indicating  that  the  activity 
of  the  right  ventricle  at  the  end  of  systole  predominates  over 
that  of  the  left,  whereas  a  downward  T,  as  recorded  by  Deriva- 
tion /.,  imphes  predominant  activity  of  the  left  ventricle. 

In  some  cardiac  affections  the  electro-cardiogram  presents 
^.bnormal  features. 

1.  Heart  Failure.— In  a  healthy  heart,  T,  as  recorded  by 
Derivation  /.,  is  always  an  upward  deflexion.     An  inverted  T 


3 


Fig.  66. 

1  and  ^  are  electro-cardiograms  by  Derivations  /.  and  ///.  from  a  case  of  mitral 
stenosis;  3  and  4  are  electro-cardiograms  by  Derivations  /.  and  III.  from  a 
case  of  aortic  incompetence. 


deflexion  (by  Derivation  /.)  is  one  of  the  most  constant  and 
reUable  electro-cardiographic  indications  of  ventricular  weak- 
ness, and  is  probably  evidence  of  relative  failure  of  the  conus 
arteriosus  of  the  right  ventricle. 

2.  Mitral  Stenosis. — Many  cases  of  mitral  stenosis  (Fig.  66: 
1,  2)  yield  electro-cardiograms  in  which  the  ventricular  de- 
flexions present  the  following  characteristic  features — namely, 
M  by  Derivation  /.  is  smaller  than  R  by  Derivation  ///.,  and 
8  by  Derivation  I.  is  larger  than  8  by  Derivation  ///.     These 


THE  ELECTRO-CARDIOGRAPH  119 

changes  are  due  to  the  predominant  hypertrophy  of  the  right 
ventricle  that  results  from  the  mitral  lesion. 

3.  Aortic  Incompetence. — In  many  instances  the  character- 
istic electro-cardiographic  features  (Fig.  66:  3,  4)  are  the 
reverse  of  those  observed  in  mitral  stenosis.  R  by  Deriva- 
tion I.  is  larger  than  R  by  Derivation  ///.,  while  8  by  Deriva- 
tion /.  is  smaller  than  8  by  Derivation  ///.  The  changes  are 
the  expression  of  predominant  hypertrophy  of  the  left  ven- 
tricle. 

4.  Defects  o£  Conduction — Heart-Block. — Dm-ing  the  in- 
terval P-Q  (or  P-R),  the  stimulus  is  being  transmitted  along 
the  conducting  system  from  auricles  to  ventricles,  and  the 
duration  of  this  interval  indicates  the  rate  at  which  the  stimulus 


IAJ.>vJp^Jl>\JJ 


Fig.  67. — Partial  Heart-Block. 

The  cervical  curve  and  the  electro -cardiogram  (Derivation  II.)  from  a  case  of 
mitral  stenosis  without  presystolic  murmur. 

is  being  conducted.  The  P-Q  or  P-R  interval  is  a  better  index 
of  the  rate  of  conduction  than  the  a-c  interval  in  a  jugular 
tracing,  for  the  electro-cardiogram  obviates  the  fallacies  of  an 
unknown  presphygmic  period  and  of  the  time  that  has  to 
elapse  between  the  opening  of  the  aortic  valve  and  transmis- 
sion of  the  pulse  wave  to  the  artery  in  the  neck. 

Minor  degrees  of  impaired  conductivity  in  the  bundle  can 
be  recognized  readily  in  electro-cardiograms.  In  Fig.  67, 
from  a  case  of  mitral  stenosis,  the  P-R  interval  measures  from 
0'28  to  0*31  second,  which  is  approximately  twice  the  duration 
of  the  P-R  interval  in  health  (0'  14  second). 

When  conductivity  in  the  auriculo-ventricular  bundle  is  still 
further  impaired,  so  that  either  partial  or  complete  heart- 
block  results,  the  defect  is  well  seen  in  electro-cardiograms. 


120 


DISEASES  OF  THE  HEART 


Fig.  68,  obtained  from  a  man  aged  seventy-five,  is  an  illustra- 
tion of  complete  heart-block.  The  auricular  deflexions,  P, 
occur  rhythmicall}^  at  a  rate  of  ninety-seven  per  minute;  the 
ventricular  deflexions  are  rhythmic  at  a  rate  of  thirty-eight 
per  minute,  and  there  is  complete  dissociation  of  the  auricular 
and  the  ventricular  rhythms . 

By  means  of  the  electro-cardiograph  a  complete  severance 
of  either  the  right  or  left  branch  of  the  bundle  may  be  recog- 


Fig.  68. — Electeo-Caediogram  from  a  Case  of  Full  Heart-Block  (Deriva- 
tion /.). 

The  auricular  rate  is  97,  the  ventricular  rate  38,  per  minute. 

nized.  When,  for  example,  the  right  branch  is  severed,  each 
auricular  stimulus  passes  to  the  two  ventricles  through  the 
left  branch  alone,  and  all  the  ventricular  deflexions  have  the 
same  characters  as  those  of  an  extra-systole  originating  in  the 
left  ventricle. 

5.  Extra-Systoles   can   be  recognized   with  great   precision 
in  electro-cardiograms.     An  auricular  extra-systole  is   repre- 


^^l^ 


Fig.  69. — Coupled  Rhythm  of  Ventricles,  due  to  kegulaely   eecuering 
Ventricular  Extra-Systoles. 

The  auricular  deflexions  P  are  rhythmic  throughout  (Derivation  //.). 

sented  by  an  initial  auricular  deflexion  which  is  premature, 
usually  of  abnormal  form,  and  often  inverted,  indicating 
that  the  beat  does  not  originate  in  the  sino-auricular  node, 
but  is  of  ectopic  origin.  This  auricular  deflexion  is  suc- 
ceeded by  ventricular  deflexions  which  are  usually  of  normal 
form. 


THE  ELECTRO-CARDIOGRAPH 


121 


A  ventricular  extra-systole  yields  an  "  atypical  "  electro- 
cardiogram because  the  stimulus  exciting  the  premature  beat 
spreads  through  the  ventricular  musculature  in  an  abnormal 
manner.  The  deflexions  representing  a  ventricular  extra- 
systole  are  usually  of  larger  amphtude  than  those  of  a  physio- 
logical beat,  and  are  in  striking  contrast  to  the  feeble  puLse- 


iiiiniiiiiiiihiiiiaauiiuiuiiiiUiiiiiiiiuiAiiiiimmiiuiiiuiiiitiiuiiiiiiiiiiiAiiiiiiiiiiiiuiii.uuiiiiuiiiiiiyuiiiiti 

Fig.  70. — AtrRicuLAR  Flutter. 

The  auricular  deflexions  are  diphasic  and  rhjiihmic,  and  number  281  per  minute. 
The  ventricular  contractions  number  70'25  (Derivation  //.). 

wave  transinitted  into  the  arteries.  Two  main  varieties  of 
ventricular  extra-systole  are  recognized:  (1)  Left  apical  extra- 
systoles,  in  which  the  deflexion  is  first  downwards  and  then 
upwards ;  and  (2)  right  basal  extra-systoles,  in  which  the  de- 
flexion is  first  upwards  and  then  downwards  (Fig.  69).  It  is 
important   to    note   that    the   first   variety   of   extra-systole, 


u^..4v.-4. 


nniiiiiiimuiiiuuimiiUiJiUiuJiiiJiiiiiiuiiiiijUiUiimiiiMMiiUiMUiiiiiiAtiiiuuiuimiuiuuiiiiiiMiiniiiiiiiiiiiiiiiiiiiiiit 


Fig.  71. — Aukicitlar  Fibkillation. 

The  auricular  deflexions  are  small,  irregular,   and  frequent, 
rhythm  is  irregular  (Derivation  //.). 


The  ventricular 


when  recorded  by  Derivation  /.,  usually  yields  the  same 
form  of  electro-cardiogram  as  does  the  second  variety 
by  Derivation  ///.,  and  that  the  latter  bj^  Derivation  I. 
presents  the  same  form  as  does  the  first  variety  by  Deriva- 
tion III. 

Nodal  extra-systoles  present  ventricular  deflexions  similar  to 


122  DISEASES  OF  THE  HEART 

those  of  a  genuine  ventricular  extra-systole,  but  tlie  auricular 
deflexion  is  also  premature,  and  may  be  inverted. 

6.  Auricular  Flutter  is  characterized  by  rhythmic  co-ordinate 
contractions  of  the  auricular  musculature  at  a  greatly  acceler- 
ated rate — usually  250  to  300  per  minute.  In  most  instances 
the  ventricles  respond  to  every  second  or  every  fourth  auricular 
beat.  Electro-cardiograms  are  extremely  helpful  in  deter- 
mining the  existence  of  auricular  flutter.  In  Fig.  70  the 
diphasic  auricular  deflexions  occur  rhythmically  at  a  rate  of 
281  per  minute ;  the  ventricles,  meanwhile,  are  beating  rhythmi- 
cally at  a  rate  of  70' 25  per  minute.  In  earher  records  from 
this  case  the  auricular  and  ventricular  rates  were  283  and 
141"  5  respectively.  After  digitahs  had  been  administered  for 
several  days  the  auricular  flutter  became  replaced  by  fibrilla- 
tion. 

7.  Auricular  Fibrillation. — As  this  subject  is  discussed  fuUy 
in  Chapter  XVII.,  one  electro-cardiogram  wiU  suffice  to  illus- 
trate the  essential  features.  Throughout  the  record  in  Fig.  71 
there  is  a  series  of  small,  rapid  deflexions,  irregular  in  time  and 
form,  characteristic  of  auricular  fibrillation.  The  record  also 
shows  the  whoUy  irregular  rhythm  of  the  ventricles  in  conse- 
quence of  the  auricular  fibrillation.  The  rate  of  the  auricular 
deflexions  in  cases  of  fibrillation  is  usually  from  400  to  600  per 
minute. 


^^Ovjv>jvJv_juCa^^ 


Fig.  72.~RBSPiRATORr  and  Pcjlse  Curves, 


;  Variations  in  the  Cahdiao  Rhythm  which  abe  sometimes 


_AAAivJvjVJVMVjviv^.JvAJ^.K 


Rhythm  of  the  Respibations. 


116    S^st. 
'^7    JJin^C 


TL___MUl)»'»'''~"™"M««n 


■WVMWWWWMWMWWWW/MWJl 


I'la.  73.— SrilYOMOMMOMKTEIO  TEiCINO,  SnOWINO  Tl 
LOWEK   PllBSSDBE   01   TUE   ExTEA-SysTOUO  BbaT, 


-^'i L     ■■■? 


i Lli I  Mt 


f^^fcS=!t 


Fio.  74.— Ihteepolatbd  Vektrioolae  Extea-Systole. 
Tho  rhythm  of  the  heart  is  otherwise  unchanged. 


Fig.  75. — Venteicdlae  Extea-Systolb. 

The  ventricular  contractiun  precedes  the  regular  auricular  contraction, 
which  is  not  succeeded  by  a  ventricular  contraction,  as  the  ventricle  is 
still  refractory. 


CHAPTER  VIII 
STIMULUS  PRODUCTION 

In  the  healthy  adult  the  pulse  beats  fairly  regularly,  and 
about  seventy  times  per  minute  when  the  individual  is  at  rest. 
In  infancy  and  childhood,  however,  the  rate  is  more  frequent, 
and  it  may  vary  very  considerably,  becoming  more  rapid  on 
exertion,  with  emotion,  and  after  the  ingestion  of  food.  The 
rhythm,  too,  is  often  irregular,  especially  during  sleep,  but 
polygraph  tracings  show  a  normal  a,  c,  v.  curve,  so  that  the  dis- 
turbance must  be  due  to  a  disordered  sinus  rhythm  in  response 
to  causes  arising  outside  the  heart. 

The  maximal  irregularities  are  associated  with  irregularity 
in  the  respiratory  phases.  The  breathing  of  a  child  at  rest 
and  during  sleep  is  often  irregular,  and  the  pulse  corresponds 
■with  this  in  a  general  way,  and  becomes  more  frequent  and 
more  regular  when  the  breathing  does  the  same.  In  adoles- 
cents, and  less  frequently  in  adults,  a  similar  irregularity  is 
not  uncommonl}'  observed,  and  it  is  important  to  recognize  its 
nature,  for  it  has  no  serious  significance.  A  diagnosis  can  be 
easily  made  on  examination,  for  the  irregularity  is  found  to 
correspond  "wdth  voluntary  irregularity  in  breathing,  and  to 
disappear  wholly  or  in  part  when  the  patient  breathes  fre- 
quently and  regularly,  or  ceases  breathing  altogether.  The 
association  is  clearly  seen  in  Fig.  72.  At  the  commencement 
of  the  tracing  the  pulse  during  quiet  breathing  is  notably 
irregular,  long  diastoles  occurring  before  each  inspiration. 
When  voluntary  apnoea  is  produced,  the  long  diastoles  are 
more  frequent;  but  diastole  is  shorter  when  the  respirations 
become  more  frequent  and  the  pulse  is  much  more  regular. 

As  a  matter  of  fact,  careful  measurement  of  normal  tracings 
in  adults  shows  that  the  regularity  of  the  cardiac  action  is 

123 


124  DISEASES  OF  THE  HEART 

apparent,  and  not  real,  though  the  rhythm  appears  regular  to 
the  finger  and  even  on  auscultation.  In  childhood  all  the 
functions  are  unstable.  Children  laugh  and  cry  on  shght 
provocation ;  their  temperature  rises  to  inordinate  heights  from 
trivial  causes ;  and  an  irregular  pulse  should  be  looked  upon  as 
an  indication  of  the  same  tendenc}^ 

In  disease  both  the  rhythm  and  the  rate  of  the  pulse  may 
vary  considerably.  The  pulse  is  almost  always  more  frequent 
in  fever,  and  it  is  often  notably  infrequent  during  convalescence 
from  acute  disease,  in  intoxications  such  as  jaundice,  and  in 
cerebral  diseases  such  as  meningitis,  haemorrhage,  and  tumour. 
In  Cheyne-Stokes  or  cyclic  breathing  the  pulse-rate  often 
varies  during  the  different  respiratory  phases  (Fig.  146),  but  the 
association  is  not  constant,  for  it  may  be  unaltered  or  more  or 
less  frequent  during,  say,  apnoea  in  different  individuals.  The 
curves,  too,  do  not  correspond,  and  the  maximal  changes  are 
not  coincident,  while  polygraph  curves  are  normal.  Irregu- 
larities of  this  kind  have  no  cardiac  significance,  and  must  be 
regarded  as  evidence  of  an  intoxication.  They  disappear  with 
improvement  in  the  other  symptoms. 

These  variations  in  the  rate  and  rhythm  of  the  pulse  are 
probably  due  to  variations  in  the  rate  and  rhythm  of  stimulus 
production,  though  they  might,  of  course,  result  from  dis- 
turbances of  excitabihty,  a  smaller  stimulus  sufficing  to  produce 
a  contraction  when  this  function  is  exalted,  and  vice  versa. 


CHAPTER  IX 
EXCITABILITY 

The  regular  sinus  rhythm  of  the  heart  may  be  at  times  inter- 
rupted by  the  occurrence  of  a  "  premature  or  extra- systole  in 
response  to  a  stimulus  arising  at  some  abnormal  site  in  the 
heart,  the  fundamental  or  sinus  rhythm  being  otherwise  main- 
tained "  (James  Mackenzie),  An  extra-systole  is  readil}^  recog- 
nized when  feehng  the  pulse,  the  regular  sequence  of  beats 
being  interrupted  by  the  occurrence  of  an  early  wave,  which 
is  followed  by  an  interval  of  longer  duration  than  the  average. 
An  extra-systohc  beat  is  always  of  smaller  volume,  of  shorter 
duration,  and  of  lower  pressure  (Fig.  73)  than  the  normal 
beat ;  for,  as  a  result  of  the  shorter  diastole,  the  ventricle  is  not 
well  filled  with  blood,  and  its  output  is,  in  consequence,  les- 
sened; its  contractility  is  not  fully  restored,  and  the  maximal 
contraction  possible  is  of  shorter  duration  and  lessened  power : 
while  the  aortic  blood-pressure  is  still  at  a  higher  level  than  is 
reached  after  an  interval  of  normal  length.  The  post-extra- 
systohc  beat,  too,  is  abnormal  as  a  rule,  being,  on  account  of  the 
prolonged  diastole,  a  larger,  stronger,  and  better  sustained  wave. 

Three  varieties  of  extra-systole  are  now  recognized — namely, 
ventricular,  auricular ,  and  nodal. 

Ventricular  Extra-Systoles. — A  ventricular  extra-systole  may 
not  interfere  with  the  normal  sinus  rhythm  (interpolated  ven- 
tricular extra-systole).  An  example  is  shown  in  Fig.  74,  where 
the  premature  wave  r'  in  the  brachial  tracing  (the  result  of  a 
contraction  of  the  left  ventricle)  corresponds  with  c'  in  the 
cervical  curve,  its  equivalent  carotid  expression,  and  c'  is 
succeeded  by  the  auricular  wave  a  at  the  usual  time.  A  con- 
traction of  the  left  ventricle  has  occurred  prematurely,  but 
otherwise  the  sinus  rhythm  remains  unaltered. 

125 


126 


DISEASES  OF  THE  HEART 


Ventricular  extra-systoles  do  not  as  a  rule  interfere  with  the 
rhythmic  beats  of  the  auricle.  In  Fig.  75  a  "sinus  "  ventricu- 
lar contraction  is  lost,  for  the  ventricle  being  aheady  in  con- 
traction as  a  result  of  the  abnormal  stimulus,  is,  in  consequence, 
refractory,  and  cannot  respond  when  the  "  normal  "  stimulus 


Fig.  76. — Vektricular  Extea-Systole. 

The  double  period  3-4  is  exactly  equal  to  twice  the  normal  pulse  period. 
The  post-extra-systolic  pause  is  fully  compensatory. 

arrives  from  the  auricle.  Ventricular  extra-systoles  may,  as 
in  this  case,  precede  an  auricular  contraction,  or  they  may 
succeed  it  or  may  occur  synchronously.  In  the  latter  case, 
since  the  auriculo-ventricular  valves  are  shut  during  ven- 
tricular systole,  the  "  wave  in  the  cervical  curve  is  large,  as 
the  contents  of  the  auricle  are  returned  into  the  jugular  vein. 


t^ 


■bS 


■ts 


•feS-       1-35  I       -7  I       -7  1-3 g  I        -7  I  7  I     -65-      |av^cPi^ 


(Xc  V  o-c   V  a-c  V  CO.  ^^a  c  vMac  v  cQu    olc  \/    a^c  w  ac  \j  ac    v 

Fig.  77. — Venteictjlar  Extra-Systole,  followed  by  an  Auriculae  Extea- 
Systole. 

The  post-extra-systolic  pause  is'short. 

The  pause  which  occurs  after  a  ventricular  extra-sj-stole  is 
as  a  rule  prolonged,  and  of  such  a  length  that,  taken  in  conjunc- 
tion with  the  pulse  period  preceding  the  extra-systole,  it  measures 
exactly  double  the  normal  pulse  period,  the  post-extra-systoHc 
ventricular  contraction  being   delayed  until  the  next  sinus 


EXCITABILITY 


127 


stimulus,  whose  rhythm  is  undisturbed,  passes  through  the 
auricle,  and  reaches  the  ventricle  (Fig.  76). 

In  certain  cases  the  post-extra-systolic  pause  is  not  fulh^ 
compensatory,  as  in  Fig.  77,  where  it  is  of  normal  length,  an 
auricular  extra-systole  succeeding  the  ventricular  extra-systole 
and  disturbing  the  sinus  rhythm.  Auricular  extra-systoles  not 
infrequently  succeed  ventricular  extra-systoles,  for  when,  as 
in  this  case,  the  auricular  and  the  ventricular  contractions 
coincide,  the  auricle  at  the  termination  of  systole  is  incom- 
pletely emptied,  and  being  rapidly  distended  during  diastole 
by  the  blood  flowing  quickly  into  it  from  the  over-distended 
vena  cava,  is  induced  to  contract  prematurely  by  the  sudden 
increase  of  pressure  within  its  cavity. 


Fig.  78. — Auricular  Extra-Systoles. 
The  a-c  interval  is  prolonged  (0"25  second)  with  the  extra- systolic  beats. 

Auricular  Extra-Systoles.  —  In  auricular  extra-systoles 
(Fig.  78)  the  premature  contraction  commences  in  the  auricle, 
and  is  followed  by  a  premature  ventricular  contraction.  As 
diastole  in  these  cases  is  short,  conductivity  is  imperfectly 
restored,  and  the  interval  between  the  auricular  and  the  ven- 
tricular contractions  is  unduly  prolonged.  The  presphygmic 
interval  and  the  transmission  time  are  also  necessarily  in- 
creased, and  the  a-c  interval  in  the  cervical  curve  exceeds  the 
normal  0-15  to  0*20  second.  The  post-extra-systohc  pause  is 
rarely  fuUy  compensatory,  for  the  sinus  rhythm  is  dis- 
turbed, its  stimulus  material  being  "  exploded  "  prematurely, 
and  the  succeeding  "sinus  "  beat  is,  in  consequence,  pre- 
mature. 

Nodal  Extra-Systoles. — The  third  form  of  extra-systole  is 
styled  "nodal  "  b}'  James  Mackenzie,  on  the  ground  that  the 
stimulus  probabl}^  arises  in  the  vicinity  of  the  a.v.  node.     A 


128 


DISEASES  OF  THE  HEART 


nodal  extra-systole  is  shown  in  Fig.  79,  where  both  the  a'  and 
the  c'  waves  are  premature. 

The  a-c  interval  in  normal  cervical  curves  measures  about 

0"15  to  0"20  second,  being  slightly 
shorter  if   the  pulse-rate  is   fre- 
quent.    During   the   a-c       terval 
five  events  occur :  (1)  The  auricular 
systole,  which  lasts  for  about  0*10 
second;    (2)    the  passage  of  the 
stimulus  from  auricle  to  ventricle ; 
(3)  the  latent  period  of  ventricular 
contraction;    (4)    the    period    of 
ventricular  systole  prior   to    the 
opening  of  the  aortic  cusps  (pre- 
sphygmic  interval) ;  (5)  the  trans- 
mission of  the  aortic  wave  to  the 
carotid  artery.  The  average  period 
between    the    commencement    of 
ventricular   systole   and  the  ap- 
pearance of   the  carotid  wave  in 
the 'neck  (4  and  5)  is  0"06  second 
(0-03  to   0-11  second),  while  the 
commencement  of  auricular  sys- 
tole practically  coincides  with  the 
appearance  of  the  a  wave  in  the 
jugulo-carotid  tracing.     The  pre- 
sphygmic  interval  and  the  trans- 
mission     time      are     invariably 
lengthened  in  premature  systoles 
(Fig.  80),  and  it  thus  seems  proba- 
ble that  whenever  the  a-c  interval 
in  the  cervical  cmve  measures  less 
than  0"10  second,  the  auricle  and 
ventricle  respond  to   a  common 
stimulus    which    arises    between 
them. 

Tracings  of  a  comparable  kind  have  been  produced  experi- 
mentally, and  Lewis  has  shown  that  in  the  cases  which  we  are 
considering  the  auricular  electric  complex  is  inverted,  resembhng 


EXCITABILITY 


129 


an  auricular  complex  produced  by  stimulation  of  the  auricular 
muscle  near  the  auriculo-ventricular  sulcus ;  while  the  ven- 


tricular complex  is  normal,  and  re- 
sembles a  ventricular  contraction  pro- 
duced by  a  stimulus  arising  near  the 
auricle. 

(The  meaning  of  an  inverted  P  is, 
however,  by  no  means  decided,  for 
Rothberger  and  Winterberg  have  shown 
that  it  may  occur  when  the  left  auricle 
commences  to  contract  before  the  right.) 

As  a  rule  in  these  cases  a'  precedes 
c',  but  sometimes  c'  precedes  a'  (Fig.  81), 
and  in  other  cases  a'  and  c'  are  inex- 
tricably mingled,  and  the  "  wave  is 
large,  for  the  auricular  contraction  is 
occurring  at  a  time  when  the  auriculo- 
ventricular  valves  are  shut,  and  the 
auricular  contents  are,  in  consequence, 
thrown  back  into  the  veins.  But  in 
all  three  varieties  the  auricular  and  the 
ventricular  contractions  are  prematuie, 
and  separated  by  an  extremely  short 
interval.  They  differ  in  this  respect 
from  auricular  extra-systoles  in  which 
the  a-c  interval  is  always  prolonged. 


\ 


Little  information  is  as  yet  available 
regarding  the  causes  of  extra-systoles. 
Experimentally  they  can  be  produced 
in  various  ways :  by  direct  application 
of  mechanical,  thermal,  electrical,  or 
chemical  stimuH ;  by  clamping  the  aorta, 
the  pulmonary  artery,  or  the  great  veins ; 
by  ligation  of  a  branch  of  the  coronary 
arteries  ;  and  by  the  injection  of  digitahn, 
adrenahn,  aconitine,  muscarine,  and 
physostigmine.  It  is  well  known  that  they  can  be  produced 
in  hearts  which  are  isolated  or  whose  nervous    connections 

9 


^  H 


A  a 

<i  a 

>  Eh 

a  O  H 

^  H  J 

s  §  <» 

S  Ch  1-1 

o  <JO 

M  « 

"  S  g 

o  o 

«  a  a 

H  a  o 

J  f^  g 

d  Q  =- 

S  5  a 

2  "^  S 

«  2  « 

<i  EH  a 

3  5  fc: 

(3  <!  g 

D  «  O 

K  H  W 

<^^ 

fe  «  ? 

o  "^  ^ 

<2g 

<  g- 

o>  IZ 

g  a  3 

t»  Eh  , 

a 


S   °   > 
t>    Eh    f^ 

o  a'^ 
S  o  a 

<I  a  EH 
Q  a    - 

5  o  tf 

;2  s  « 

M  a  Si 
CO  mpq 


130 


DISEASES  OF  THE  HEART 


m 

kin 


are  wholly  severed,  so  that  it  seems  that  the  cause  must  be 
sought  for  in  the  heart  itself. 

The  direct  apphcation  of  stimuli  to  excitable  muscle  natur- 
ally provokes  a  contraction ;  the  obstruction  of  a  great  artery" 

produces  over-distension  of  the  cavities 
behind  the  block,  and  provides  a 
mechanical  stimulus ;  ligation  of  a 
coronary  branch  interferes  with  the 
nutrition  of  the  part  concerned  bj^ 
reason  of  the  ischsemia  which  follows ; 
and  the  injection  of  drugs  involves  a 
chemical  as  well  as  a  mechanical  stimu- 
lus. But  it  is  well  known  that  an 
extra-systole  has  per  se  no  serious 
prognostic  significance.  Extra-systoles 
occur  at  all  ages,  though  they  are  least 
common  in  childhood,  and  in  hearts, 
which  are  apparently  normal  as  well 
as  in  those  which  are  obviously 
diseased;  and  it  is  difficult,  in  conse- 
quence, to  understand  the  mechanism 
by  which  they  are  produced  during 
hf  e,  though  it  must  be  somewhat  simi- 
lar to  those  which  have  been  utilized 
in  experiment. 

As  a  general  rule,  the  type  of  extra- 
systole  in  any  particular  individual,, 
whether  it  is  auricular,  ventricular,  or 
nodal,  remains  constant;  and  extra- 
systoles  can  often  be  produced  at  will 
in  persons  in  whom  they  occur  spon- 
taneously by  slight  physical  exertion, 
or  by  the  cessation  of  respiration.  In 
a  general  way,  again,  extra-systoles 
are  most  common  in  cases  with  myo- 
cardial changes,  the  result  of  acute 
rheumatic  endocarditis  or  chronic  disease  of  the  coronary^ 
arteries,  and  they  are  frequently  present  in  the  later  stages 
of   acute   endocarditis   at   a    time  when   submihary  nodules 


T 


—  Y 


-4 


^  .2 


EXCITABILITY  131 

are  being  formed.  It  seems  probable  that  in  many  cases  some 
local  lesion  has  produced  a  local  hyper-irritability  which 
induces  a  premature  contraction  in  response  to  stimuli  of 
minimal  degree. 

This  inference  is  supported  by  some  of  the  phenomena  which 
are  associated  with  heart-block  and  nodal  rhythm. 

In  chronic  heart-block  the  ventricular  rhythm  is  infrequent 
and  fairly  regular,  but  in  the  early  stages  the  pulse  may  be 
extremely  irregular,  a  series  of  beats  in  rapid  succession  alter- 
nating with  contractions  that  occur  at  widely  spaced  intervals 
(Fig.  102).  The  scar  of  the  lesion  which  has  interrupted  the 
passage  of  the  stimuK  is  unirritating,  and  the  inherent  ven- 
tricular rhythm  comes  into  action  in  the  chronic  cases ;  but  in 
the  acute  stages  the  connective-tissue  hyperplasia  is  irritant, 
and  now  provokes  frequent  contractions,  now  inhibits  aU  con- 
tractions for  a  time.  A  comparable  phenomenon  has  been 
noticed  in  nodal  rhythm,  nodal  extra-systoles  preceding  the 
onset  of  the  rhythm.  The  irritation  of  the  node  at  first 
produced  occasional  ectopic  beats,  but  eventually  every  con- 
traction, the  sinus  influence  becoming  effaced. 

The  pressure  within  the  chambers  of  the  heart  is  constantly 
varying  with  the  varying  phases  of  systole  and  diastole,  with 
the  respiratory  movements,  and  with  physical  exertion,  and 
it  is  known  that  elevation  of  the  pressure  within  the  heart  may 
evoke  ectopic  beats.  It  seems  probable  that  they  are  often 
due  to  such  causes,  a  prior  lesion  having  rendered  some  part 
unduly  irritable. 

In  other  cases,  however,  the  irritabihty  is  probably  of 
functional  origin.  The  cardiac  rhythm  is  unstable  in  fever, 
and  the  pulse-rate  alters  notably  from  causes  (emotion,  exer- 
tion) which  in  a  healthy  individual  would  produce  httle  change. 
Extra-systoles  are  not  uncommon  in  those  diseases,  and  may 
be  due  to  a  heightened  general  irritability  induced  by  the 
fever,  toxaemia,  etc.,  rather  than  to  local  lesions  within  the 
muscle,  though  these  are  often  present  even  in  the  absence  of 
endocarditis.  Extra-systoles,  too,  may  occur  in  persons  who 
are  suffering  from  alcohohc  or  nicotine  poisoning,  cr  from  the 
metabolic  disturbances  associated  with  the  presence  of  uric 
acid  or  oxalates  in  excess  in  the  urine,  and  they  tend  to  dis- 


132  DISEASES  OF  THE  HEART 

appear  when  the  intoxication  is  remedied.  In  these  diseases 
the  blood-pressure  is  generally  elevated,  and  as  Knoll  and 
Hering  have  shown  that  ectopic  beats  can  be  produced  by 
reflex  disturbance  of  the  vasomotor  centres,  the  association  is 
extremely  suggestive. 

The  cKnical  significance  of  extra-systoles  thus  varies  in  dif- 
ferent cases.  In  acute  endocarditis  they  may  be  regarded  as 
probable  evidence  of  myocarditis,  and  thus  of  somewhat  serious 
import.  In  other  diseases  they  indicate  a  local  or  a  general 
hyper-irritability  of  the  heart,  and  careful  search  should  be 
made  for  its  cause.  In  the  absence  of  any  sign  of  cardiac 
insufficiency,  the  immediate  prognosis  is  good ;  but  every  effort 
should  be  made  to  discover  the  source  of  the  irritation,  and.  if 
possible,  to  remove  it.  There  is  a  general  feeling  that  auricular 
extra-systoles  have  a  more  serious  significance  than  the  ven- 
tricular forms,  but  the  evidence  as  yet  is  inconclusive.  Nodal 
extra-systoles  should  probably  be  placed  with  the  auricular 
group  as  regards  their  import. 


CHAPTER  X 
NODAL  RHYTHM 

In  certain  cases  the  rhythm  of  the  heart  seems  to  be  set  by 
stimuli  arising  in  the  vicinity  of  the  a.v.  node  (James  Mac- 
kenzie), for  every  beat  shows  a  greatly  shortened  a-c  interval 
(c/.  p.  127,  Nodal  Extra-Systole).  The  rhythm  is  regular,  but 
the  pulse-rate  varies  in  different  cases,  being  sometimes  very 
frequent  (over  200),  and  more  rarely  normal  or  but  shghtly 
increased.  Two  groups  can  be  recognized:  in  one  the  rhythm 
is  intermittent  and  paroxysmal,  alternating  with  a  rhythm  of 
normal  type  (paroxysmal  tachycardia  of  the  auricular  form; 
c/.  Chapter  XV.) ;  in  the  other  the  new  rhythm  is  permanent. 

The  onset  and  the  cessation  of  the  paroxysms  in  the  first 
group  are  practically  instantaneous,  and  they  may  recur  at 
varying  intervals  and  last  for  varying  periods,  sometimes  for 
but  a  few  seconds,  sometimes  for  hours  or  even  days.  In  the 
second  group  the  rhythm  continues  indefinitely. 

I  have  observed  seven  examples  of  the  second  group.  In 
six  of  these  patients,  who  were  suffering  from  acute  endo- 
carditis, we  were  able  to  examine  the  hearts  after  death,  and 
serial  sections  of  the  a.v.  node  and  bundle  (A.  M.  Kennedy) 
showed  that  the  node  was  the  site  of  an  inflammatory  disturb- 
ance which  seemed  sufficient  to  account  for  its  undue  excita- 
bility. 

The  first  two  cases  are  recorded  elsewhere  in  detail,  Case  1 
on  p.  246,  and  Case  2  on  p.  240. 

Case  3. — The  patient,  a  man  aged  forty-two,  was  admitted 
to  hospital  on  January  31,  1911,  complaining  of  breathlessness 
and  of  swelling  of  the  feet  and  legs  of  some  six  months'  dura- 
tion. 

He  had  always  enjoyed  good  health  prior  to  the  onset  of  his 

133 


134  DISEASES  OF  THE  HEART 

illness,  save  for  pneumonia  at  the  age  of  thirty,  and  attacks  of 
measles  in  childhood  and  at  the  age  of  thirty- two.  He  had 
habitually  used  tobacco  and  alcohol  to  excess. 

In  the  preceding  April  he  had  caught  cold,  and  had  never 
been  weU  since.  The  cough  and  spit  persisted,  and  he  lost 
appetite  and  felt  weak  and  unable  to  do  his  work.  In  July 
he  noticed  that  his  feet  were  sometimes  swollen  at  night,  and 
he  began  to  be  very  breathless  on  exertion.  In  August  the 
oedema  became  permanent,  and,  steadily  increasing  in  amount, 
soon  compelled  him  to  remain  in  bed.  In  December  he  one 
day  suddenly  felt  severe  pain  in  his  right  side,  and  spat  blood 
in  considerable  quantities  for  some  weeks.  He  had  to  be 
propped  up  in  bed  on  account  of  breathlessness,  the  spit  and 
the  oedema  steadily  increased  in  amount,  and  his  general 
strength  rapidly  failed.  In  January  he  attempted  a  short 
walk,  but  fell  down  in  a  faint  on  the  pavement. 

On  admission,  the  patient  was  extremely  ill.  He  sat  bolt 
upright  in  bed,  coughing  continually  and  spitting  up  large 
quantities  of  watery  mucoid  material.  CEdema  was  universal, 
and  very  marked  in  the  legs  and  scrotum.  Detailed  examina- 
tion was  impossible,  but  evidence  was  found  of  a  consolidation 
of  the  middle  lobe  of  the  right  lung  and  of  pleurisy  on  the 
same  side.  The  heart  was  enlarged,  and  double  aortic  mur- 
murs were  audible  over  the  sternum.  Progress  was  con- 
tinually in  the  wrong  direction.  The  hsemoptysis  recurred, 
the  dyspnoea  and  oedema  increased,  exhaustion  became  more 
and  more  extreme,  and  he  died  suddenly  on  February  5. 

The  respiratory  difficulty  prevented  continuous  observation 
of  the  cardiac  irregularities.  The  pulse  on  admission  was 
notably  irregular  in  rhj^thm  from  the  frequent  occurrence  of 
extra-systoles,  but  a  series  of  twenty  or  thirty  fairly  regular 
beats  of  slow  rate  occasionally  obtained.  The  extra-systoles 
were  sometimes  isolated  and  sometimes  in  salvos  of  two,  three, 
or  four.  On  February  1  the  same  state  continued.  On  the 
2nd  the  pulse  was  very  irregular  and  very  mobile,  a  bout  of 
coughing  quickening  the  rate  from  about  90  to  about  120  to  130, 
the  frequent  rate  persisting  for  a  minute  or  two  after  the 
cough  ceased.  On  the  3rd  the  irregularity  was  more  marked, 
but  on  the  4th  had  disappeared,  the  pulse  being  quite  regular. 


NODAL  RHYTHM  135 

with  a  rate  of    110  to  120.     Alternation  was  distinct.     The 
rhythm  remained  regular  until  death. 

Cervical  curves  were  only  obtained  on  February  2  and  4, 
and  were  somewhat  deformed  by  the  respiratory  movements. 
Tracings  on  the  2nd  demonstrated  that  while  the  a-c  interval 
in  the  case  of  the  larger  beats  was  of  normal  length,  it  was 
much  shorter  with  the  extra-systoles,  varying  between  O'lO 
and  0"15  second.  On  the  4th,  when  the  rhythm  was  regular 
but  more  frequent,  the  a-c  interval  was  always  short,  and 
measured  0*10  second  (Fig.  82).  The  tracings  thus  seem  to 
show  that  on  the  2nd  extra-systoles  were  arising  in  the  vicinity 
of  the  node,  the  sinus  rhythm,  however,  on  the  whole  pre- 


1  ■'  I         a-c 

C-iJ.H^vO'H  .  4.ii'.lO. 

Fig.  82. 

Case  3:  The  pulse  is  regular,  and  the  a-c  interval  measures  0' 10  second- 
Respiratory  movements  deform  the  cervical  curve  in  places. 

dominating ;  while  on  the  4th  the  pacemaker  had  changed,  the 
sinus  influence  had  been  lost,  and  every  contraction  originated 
in  the  auriculo-ventricular  node. 

On  post-tnortem  examination  the  heart  was  found  to  be 
greatly  enlarged,  weighing  25|  ounces.  The  aortic  valve  was 
incompetent,  the  septal  cusp  having  a  fairly  large  perforation 
with  well-defined  margins  a  little  below  its  free  border.  All 
the  cusps  showed  some  small  recent  warty  vegetations,  but 
were  not  thickened.  The  other  valves  were  not  affected,  but 
the  auriculo  -  ventricular  valves  were  incompetent.  Two 
patches  of  superficial  mural  fibrosis  were  present  in  the  left 
ventricle.  One,  which  was  small,  was  situated  near  the  apex ; 
the  other,  which  measured  about  |  inch  in  diameter,  was 
situated  on  the  interventricular  septum  underneath  the  an- 
terior mitral  cusp,  its  anterior  border  being  fully  |  inch  behind 
the  posterior  border  of  the  pars  membranacea.  The  coronary 
arteries  and  the  aorta  showed  little  abnormality. 


136  DISEASES  OF  THE  HEART 

A  small  abscess  was  found  in  the  middle  lobe  of  the  right  lung 
as  well  as  a  large  infarction;  both  pleurse  were  adherent.  The 
Hver  was  adherent  to  the  diaphragm,  and  there  was  a  well- 
marked  perisplenitis.  The  kidneys  showed  slight  evidences  of 
arterio-sclerotic  fibrosis,  and  one  or  two  small  infarcts. 

Microscopic  examination  of  the  heart  showed  that  the  a. v. 
node  was  involved  in  an  acute  inflammatory  process.  Many 
focal  cellular  collections  were  present,  and  some  small  diffuse 
infiltrations,  the  muscular  fibres  in  their  vicinity  showing 
granular  degeneration.  The  reaction  was  best  marked  in  the 
upper  portion  of  the  node,  and  in  the  parts  which  were  nearest 
to  the  base  of  the  mitral  valve.  The  cells  were  chiefly  mono- 
nuclear, and  mainly  lymphocytes,  with  only  an  occasional 
polymorphonuclear  leucocyte.  The  a.v.  bundle  was  not  de- 
finitely affected,  but  was  slightly  implicated  by  a  nodule  in 
the  cardiac  muscle  immediately  beneath  and  posterior  to  it. 
The  fibrous  tissue  around  the  bundle  appeared  excessive  in 
amount,  and  showed  traces  of  calcification.  The  s.a.  node  was 
normal. 

The  cardiac  muscle  throughout  showed  evidences  of  cloudy 
swelling  and  a  few  inflammatory  "  nodules,"  which  were  most 
numerous  at  the  base  of  the  mitral  valve  and  in  the  auricular 
muscle  just  above  the  node. 

Case  4. — The  patient,  a  girl  aged  ten,  was  admitted  to 
hospital  on  June  10,  1911,  ccmplaining  of  shortness  of  breath 
and  of  swelling  of  the  feet  of  a  week's  duration. 

The  girl  had  enjoyed  good  health,  with  the  exception  of 
three  attacks  of  "measles,"  until  about  two  months  before 
admission,  when  she  was  noticed  to  be  taking  her  food  badly, 
to  be  losing  flesh,  and  to  be  disinchnecl  for  her  usual  pla3^  She 
continued,  however,  to  go  to  school  until  the  beginning  of 
June,  when  she  contracted  a  cough  unaccompanied  by  spit, 
and  became  short  of  breath  on  exertion.  Her  face  and  feet 
were  noticed  to  be  swollen,  and  she  complained  of  pain  in  the 
abdomen  and  beneath  the  sternum  when  she  coughed.  She 
had  sometimes  to  sit  upright  in  bed  at  night  on  account  of 
dyspnoea,  and  in  the  mornings  she  complained  of  headache. 

On  admission  the  child  looked  ill  and  exhausted,  and  was 
inclined  to  be  drowsy.     The  face  was  palhd  and  looked  puffy, 


NODAL  RHYTHM  137 

but  there  was  no  oedema.  The  tongue  was  thickly  coated, 
and  the  tonsils  were  sHghtly  hypertrophied.  Both  hearts  were 
enlarged,  and  there  was  pulsation  in  the  second,  third,  fourth, 
fifth,  and  sixth  left  interspaces,  the  apical  impulse  in  the  fifth 
space  being  diffuse.  A  long,  soft,  blowing  murmur  was  audible 
at  the  apex,  partly  replacing  and  partly  following  the  first 
sound,  while  the  second  sound  was  "  doubled."  Over  the 
xiphoid  the  systoHc  murmur  was  loud  and  harsh,  and  resembled 
a  friction  sound. 

During  the  next  fortnight  the  patient's  general  condition 
improved  shghtly,  but  she  still  looked  ill  and  exhausted,  and 
complained  at  times  of  substernal  pain.  An  urticarial  rash 
appeared  upon  the  24th,  and  persisted  for  a  few  days.  On  the 
29th  pericardial  friction  was  well  marked,  and  a  small  pleural 
effusion  was  discovered  at  the  base  of  the  left  lung.  In  the 
beginning  of  July  the  symptoms  became  more  serious,  and  she 
grew  steadily  weaker,  and  sometimes  sweated  profusely  at 
night.  A  crop  of  minute  subcutaneous  nodules  developed  on 
the  backs  of  the  hands,  and  persisted  for  a  few  days.  On  the 
14th  vomiting  set  in,  and  continued  severely  for  the  next  three 
days.  Exhaustion  became  more  extreme,  and  she  died  on 
July  22. 

The  nature  of  the  infection  was  obscure.  There  was  no 
history  of  arthritis,  and  the  joints  were  never  swollen  or  painful 
during  her  residence,  and  the  tonsils,  though  large,  were  not 
acutely  inflamed.  She  was  habitually  slightly  fevered  at  night, 
but  the  temperature  only  once  rose  above  101°  F.,  and  was 
more  usually  under  100°.  The  leucocyte  counts  varied  be- 
tween 8,000  and  23,000.  No  other  focus  of  infection  was  dis- 
covered, and  the  symptoms  seemed  to  point  to  a  rheumatic 
infection  of  the  heart  without  arthritis. 

The  pulse  on  admission  was  regular,  small,  and  extremely 
soft.  At  first  the  rate  was  100  to  110,  but  it  steadily  increased, 
and  for  the  last  two  weeks  of  her  illness  never  ran  below  120, 
though  it  only  numbered  140  on  two  occasions.  Tracings 
were  frequently  obtained,  and  were  regular  and  normal 
until  July  3,  when  a  ventricular  extra-systole  was  recorded. 
During  the  succeeding  days  the  pulse  was  often  shghtly  ir- 
regular from  extra-systoles,  but  no  satisf actor}'  curves  were 


138  DISEASES  OF  THE  HEART 

obtained  until  July  17  (Fig.  83).  The  respiratory  movements 
were  frequent,  and  deformed  ( + )  every  alternate  pulse-beat, 
but  a,  c,  v  are  distinct  in  the  intervening  contractions,  and  the 
a-c  interval  regularly  measures  O'lO  second.  A  tracing  on 
July  22  again  showed  a  regular  pulse,  with  an  a-c  interval  of 
the  same  length. 

Post-mortem  examination  revealed  a  well-marked  subacute 
pericarditis,  the  two  layers  of  the  pericardium  being  closely 
adherent  to  each  other  over  the  front  of  the  heart  by  fibrinous 
adhesions,  but  only  slightly  over  the  posterior  surface.  The 
parietal  pericardium  was  adherent  in  several  places  to  the 
chest  wall.  The  heart  generally  was  enlarged.  The  mitral 
and  tricuspid  valves  were  both  dilated,  and  showed  rows  of 
recent  pearly  vegetations  upon  their  auricular  surfaces. 


Fig.  83. 

Case  4:  The  pulse  is  regular,  and  the  a-c  interval  regularly  measures  O'lO  second. 
Respiratory  movements  deform  the  cervical  curve  in  places. 

One  or  two  caseous  glands  were  found  at  the  root  of  the 
right  lung.  Both  pleurae  showed  evidences  of  subacute 
pleurisy. 

Microscopic  examination  of  the  heart  showed  a  well-marked 
interstitial  myocarditis.  The  nodules  varied  somewhat  in 
their  character.  The  majority  were  composed  of  mononuclear 
cells,  with  a  few  polymorphonuclear  leucocytes ;  others  were 
of  the  "  rheumatic  "  type,  consisting  chiefly  of  multinucleated 
giant  cells,  with  only  an  occasional  lymphocyte ;  and  a  few  were 
"  mixed  "  with  a  few  giant  cells,  many  lymphocytes,  and  an 
occasional  polymorphonuclear  leucocyte.  The  muscle  cells  in 
the  vicinity  were  evidently  degenerate. 

The  lesions  were  most  extreme  in  the  neighbourhood  of  the 
mitral  and  tricuspid  valves.  The  a.v.  bundle  was  involved  in 
a  large  focus  which,  occurring  near  the  tricuspid  valve,  infil- 


NODAL  RHYTHM  139 

trated  the  bundle  for  a  short  distance.  The  a.v.  node  was 
notably  affected;  none  of  the  infiltrating  cells,  however,  were 
multinucleated.  The  capillaries  were  extremely  congested,  and 
the  lymphatic  vessels  could  be  seen  plugged  with  solid  masses 
of  lymphocytes.  The  principal  vein  of  the  node  showed  an 
acute  phlebitis  and  periphlebitis.  The  greater  part  of  the 
phlebitis  was  above  the  node.  Just  before  the  vein  left  the 
node  it  was  joined  by  a  moderately  large  branch,  and  the  vein 
above  the  junction  was  thrombosed.  The  thrombus  was 
attached  to  the  side  of  the  vein,  but  did  not  completely  occlude 
it,  and  could  be  traced  through  several  sections.  The  s.a.  node 
was  not  examined. 

Case  5. — A  married  woman,  aged  twenty-seven,  was  ad- 
mitted into  hospital  on  March  12,  1910,  suffering  from  acute 
arthritis  of  about  a  fortnight's  duration.  Her  previous  health 
had  been  good,  save  for  an  attack  of  "  rheumatics  "  at  the 
age  of  seventeen,  which  involved  the  feet  and  ankles,  and  per- 
sisted in  varying  intensity  for  nearly  a  year,  though  she  was 
never  acutely  ill. 

Her  illness  had  commenced  abruptly  with  feverish  symp- 
toms on  February  23,  and  next  day  several  joints  were  swollen 
and  painful.  The  arthritis  continued,  and  she  slept  badly  at 
night  on  account  of  the  pain,  and  for  a  week  before  her  admis- 
sion had  been  short  of  breath  even  when  lying  quietly  in  bed. 

She  was  a  poorly  nourished  woman  of  medium  size,  and 
looked  exhausted.  Many  joints  were  inflamed  and  swoUen, 
and  she  was  fevered  and  sweated  profusely.  There  was  no 
cyanosis  or  oedema.  The  tongue  was  moist  and  raw,  and 
digestion  was  good.  There  was  considerable  catarrh  in  the 
chest,  and  a  small  patch  of  consolidation  at  the  extreme  left 
base. 

Improvement  at  first  was  considerable,  and  within  a  week 
the  arthritis  had  subsided,  but  the  pyrexia  continued ;  and  on 
March  18  she  had  three  attacks  of  dyspnoea,  during  which  the 
pulse  became  very  small  and  weak.  By  the  end  of  the  month, 
however,  improvement  was  definite,  and  the  chest  was  nearly 
clear.  But  in  the  second  week  of  April  the  arthritis  recurred, 
and  many  small  subcutaneous  nodules  Avere  discovered  on  the 
hands  and  elbows.     The  arthritis  subsided  within  a  few  days, 


140  DISEASES  OF  THE  HEART 

but  on  April  28  she  suddenly  complained  of  pain  in  the  front 
of  the  chest,  and  pericardial  friction  was  discovered.  A  large 
effusion  developed,  and  she  became  very  gravely  ill,  the  cardiac 
weakness  being  extreme  and  accompanied  by  widespread 
bronchitis ;  but  in  a  week  improvement  was  obvious,  and  her 
progress  thereafter  was  good.  The  arthritis  recurred  in  June, 
and  was  accompanied  by  dry  pleurisy  on  the  right  side,  but 
the  symptoms  passed  away  in  a  few  days.  Another  recur- 
rence of  arthritis  occurred  in  July,  this  time  of  trivial  degree 
and  of  short  duration.  She  left  hospital  on  account  of  domestic 
trouble  in  September,  1910. 

The  heart  on  her  admission  was  of  normal  size,  but  a  systolic 
murmur  replacing  and  succeeding  the  first  sound  was  audible 
at  the  apex.  During  the  recmTence  of  the  arthritis  in  April 
the  heart  became  notably  dilated,  and  with  the  onset  of  peri- 
carditis the  pulse  became  very  frequent  and  soft,  and  the 
cardiac  sounds  were  very  faint  and  distant.  She  was,  too, 
extremely  breathless  when  she  was  moved  in  bed.  In  June, 
however,  the  dilatation  lessened,  but  the  right  heart  was  stiU 
large  when  she  left  hospital.  The  pulse  was  of  fair  quality, 
but  habitually  ran  between  90  and  100. 

The  case  at  first  presented  some  difficulty  in  diagnosis,  for 
the  fever  which  was  present  on  admission  persisted  after  the 
arthritis  had  subsided,  and  lasted  in  greater  or  less  degree 
until  the  middle  of  May.  It  was  associated  with  a  leucocj^- 
tosis,  which  varied  from  16,000  to  26,000.  The  only  visceral 
abnormahty  at  first  was  the  mitral  lesion,  but  the  recurrence 
of  the  arthritis  and  the  occurrence  of  pericarditis  and  sub- 
cutaneous nodules  indicated  a  persistent  rheumatic  infection. 
Blood-cultures  were  sterile. 

She  continued  in  good  health  for  a  year  after  leaving  hos- 
pital, but  then  began  to  suffer  from  pains  in  her  ankles  and 
shoulders.  In  October,  1911,  she  gave  birth  to  a  healthy  baby. 
She  made  a  good  recovery  from  the  confinement,  which  was 
easy  and  uncomplicated,  and  nursed  the  child  satisfactorily 
until  February  10,  1912,  when  the  right  shoulder  became 
painful,  and  she  had  to  take  to  bed.  She  was  evidently  fevered 
at  this  time,  and  on  February  19  commenced  to  cough  and 
became  very  breathless.     She  was  again  admitted  to  hospital 


NODAL  RHYTHM  141 

on  February  22.  She  was  now  seriously  ill,  with  a  flushed, 
anxious  countenance.  The  right  \vrist  was  swollen  and  pain- 
ful. The  lower  part  of  the  right  lung  was  consolidated,  and 
there  was  a  profuse  muco-purulent  spit.  The  heart  was  en- 
larged, and  the  mitral  murmur  persisted.  The  pulse  was 
fairly  large  and  quite  regular,  but  frequent  ( 104  to  1 12),  and  was 
soft  and  quick. 

Her  progress  afterwards  was  unsatisfactory,  though  for  a 
few  days  towards  the  end  of  March  some  improvement  oc- 
curred. She  was  very  breathless,  and  had  to  sit  up  in  bed; 
the  fever  persisted,  she  sweated  profusely  and  became  very 
weak.  The  pneumonia  at  the  right  base  cleared  up,  but 
coincidently  spread  to  the  upper  and  middle  lobes.  The  knees 
and  wrists  became  swollen  and  painful  for  a  few  days.  On 
April  9  she  had  an  attack  of  faintness,  from  which  she  ralUed 
with,  difficulty,  and  faints  recurred  on  several  occasions,  though 
there  seemed  little  change  in  the  cardiac  condition,  save  that 
the  pulse  became  steadily  less  full  and  more  quick,  though  its 
rate  was  but  little  increased.  CEdema  made  its  appearance  in 
the  feet  and  at  the  bases  of  the  lungs,  and  she  died  from  cardiac 
failure  on  April  15,  1912.  The  pulmonary  affection  prevented 
accurate  observations  of  the  cardiac  sounds. 

Her  temperature  throughout  was  habitually  febrile,  but  was 
generally  remittent.  The  usual  daily  maximum  was  between 
100°  and  102°  P.,  but  on  one  occasion  103' 6°  was  touched. 
The  pulse  was  always  regular,  and  ranged  between  110  to  120, 
reaching  140  on  those  occasions  when  the  temperature  was 
high.     The  maximum  leucocyte  count  was  20,400. 

The  cervical  curves  which  were  obtained  during  her  first 
residence  were  always  normal.  During  her  second  residence 
the  curves  at  first  were  normal,  but  on  March  16,  1912,  the 
a-c  interval  was  short,  and  on  March  17  (Fig.  84)  and  subse- 
quently measured  O'lO  second  or  less,  save  for  an  isolated 
curve  on  April  4,  which  seemed  to  show  a  slightly  greater 
duration.  The  apex  tracings  showed  a  very  short  A.V.  in- 
terval (0'06  second). 

Post-mortem  examination  showed  a  patchy  pneumonia  of  the 
right  lung,  which  was  most  extensive  in  the  middle  lobe,  and 
much  passive  venous  congestion  of  lungs,  liver,  and  spleen. 


142  DISEASES  OF  THE  HEART 

The  cortex  of  the  kidneys  was  narrowed,  the  capsules  were 
thickened  and  adherent,  and  the  surface  was  markedly  granu- 
lar.    The  arteries  were  slightly  thickened. 

The  pericardium  was  uniformh^  thickened,  and  the  two 
layers  were  everywhere  adherent.  There  was  a  slight  medias- 
tinitis.  The  heart  was  greatly  enlarged  and  hypertrophied. 
The  aortic  valve  was  incompetent,  and  the  mitral  valve  was 
sHghtly  narrowed,  their  cusps  being  sHghtly  thickened  from 
chronic  endocarditis.  The  chordse  and  the  tips  of  the  musculi 
papillares  were  also  thickened  and  fibroid.  Fresh  granulations 
were  present  on  both  valves,  and  also  on  the  tricuspid,  the 
largest  being  on  the  aortic  cusps.  The  coronarj'  arteries  were 
healthy. 

The  tissues  in  the  vicinity  of  the  a.v.  system  were  examined 
microscopically  in  esrial  section.     An  extensive  fibrosis  was 


CC    V      CC    V      CC  V 


Fig.  84. 
Case  5.  The  pulse  is  regular,  and  the  a-c  interral  measures  less  than  O'lO  second. 

present  at  the  base  of  the  mitral  valve,  dense  fibrous  tissue 
spreading  from  the  valve  right  up  to  the  a.v.  node,  which  was 
traversed  by  several  narrow  strands  between  Avhich  there  were 
many  fibroblasts  and  round  cells.  The  cellular  infiltration 
extended  above  and  beyond  the  node  into  the  muscle  of  the 
auricle.  Around  the  artery  of  the  node  there  was  well-marked 
periarterial  fibrosis,  which  in  one  part  was  ver}-  thick  and  dense, 
surrounding  the  artery  like  a  collar.  The  a.v.  bundle  was  not 
involved,  though  its  arteries  were  affected  by  periarterial 
thickening.  The  s.a.  node  was  normal,  though  an  enlarged 
gland  was  adherent  to  the  pericardium  immediately  over  it. 
The  vagus  nerves  were  normal. 

The  lesions  found  were  evidently  of  different  date,  and  it 


NODAL  RHYTHM  143 

seems  probable  that  those  of  older  date  were  the  result  of  the 
illness  two  years  before  death.  The  more  recent  lesions,  too, 
were  evidently  of  some  standing,  as  fibroblasts  were  numerous 
in  the  cellular  infiltrations,  a  fact  which  may  be  correlated  to 
the  appearance  of  nodal  rhythm  a  month  before  death.  The 
node  had  evidently  been  acutely  inflamed  in  1910,  but  no 
evidence  of  a  new  rhythm  was  obtained  at  that  time;  and  in 
February,  1912,  the  cervical  curves  were  normal,  so  that  it 
appears  that  the  sinus  rhythm  was  then  predominant.  The 
attacks  of  dyspnoea  on  March  18,  1910,  however,  suggested  a 
cardiac  cause,  and  may  have  been  due  to  involvement  of  the 
node  and  the  inception  of  a  temporarj^  nodal  rhythm.  Tracings, 
however,  were  not  obtained  at  this  time. 

Case  6. — 'A  weU-grown  girl,  aged  fifteen,  who  had  had  no 
serious  illness  of  any  kind,  contracted  rheumatic  fever  in 
December,  1910,  which  confined  her  to  bed  for  two  months. 
In  April,  1911,  an  attack  of  chorea  supervened,  for  which  she 
was  admitted  into  hospital.  The  movements  ceased  com- 
pletely after  five  weeks,  and  she  was  sent  to  a  convalescent 
home,  but  a  week  after  her  return  to  her  own  home  in  the  end 
of  June  the  movements  recurred.  The  attack  was  not  severe^ 
and  she  was  dismissed  from  hospital  in  the  second  week  of 
August,  She  remained  in  good  health,  and  worked  regularly 
in  a  laundry  until  November  8,  when  a  second  attack  of  acute 
rheumatism  occurred,  for  which  she  was  at  once  admitted  to 
hospital.  The  arthritis  lasted  for  three  weeks,  and  she  seemed 
to  be  convalescent;  but  it  recurred  for  a  few  days  in  the  first 
week  of  Januar}',  1912,  and  again  in  the  first  week  of  March. 
In  the  middle  of  April  an  attack  of  pericarditis  with  consider- 
able effusion  occurred.  She  was  at  this  time  very  iU,  with 
distinct  evidences  of  cardiac  weakness ;  but  she  eventually 
improved  somewhat  rapidly,  and  she  was  allowed  to  go  to  her 
own  home  in  the  end  of  August. 

She  remained  in  fair  health  during  the  autumn,  and  was 
able  to  do  hght  housework  without  distress,  but  on  Novem- 
ber 24,  1912,  she  was  suddenly  seized  with  acute  pain  in  the 
left  chest,  which  was  aggravated  by  respiration  and  accom- 
panied by  cough  and  a  bloody  spit.  She  became  extremely 
short  of  breath,  and  vomited  repeatedl}'  and  had  to  take  to 


144  DISEASES  OF  THE  HEART 

bed.  The  pain  and  sickness  disappeared  in  two  or  three  days, 
but  the  dyspnoea  continued,  and  she  experienced  discomfort 
over  the  front  of  the  chest,  and  had  to  sit  upright  in  bed.  The 
haemoptysis  ceased  within  a  fortnight,  but  the  other  symptoms 
persisted,  and  a  week  later  oedema  made  its  appearance  in  the 
feet,  and  rapidly  spread  upwards.  She  was  again  admitted  to 
hospital  on  December  31.  She  was  now  extremely  ill,  in  full 
orthopncea,  with  small  amounts  of  fluid  in  the  serous  sacs  and 
universal  oedema,  which  was  very  great  in  the  legs.  The  liver 
was  enlarged  and  tender. 

The  symptoms  steadily  increased  in  severity,  and  more 
pulmonary  infarctions  ensued.  Towards  the  end  of  January, 
1913,  active  delirium  ensued,  and  she  slept  badly  and  took 
little  nourishment.  The  leucocyte  count  rose  to  17,500.  She 
died  somewhat  suddenly  on  February  3,  1913,  some  twenty- 
five  months  after  her  initial  rheumatic  attack. 

On  her  first  admission  in  April,  1911,  the  heart  was  of  normal 
size,  but  a  systohc  murmur  running  out  of  the  first  sound  for  a. 
considerable  distance  into  the  short  pause  was  audible  at  the 
apex.  During  her  second  residence  in  June,  1911,  the  val- 
vular lesion  seemed  unaltered,  but  on  her  admission  i'n  Novem- 
ber, 1911,  the  heart  was  dilated,  though  it  regained  its  former 
dimensions  within  a  month.  In  the  middle  of  December  a 
new  diastoUc  murmur  of  aortic  distribution  made  its  appear- 
ance, and  in  March,  1912,  double  murmurs  were  apparent  over 
the  sternum.  The  heart  was  now  definitely  enlarged,  and 
after  the  subsidence  of  the  pericarditis  the  area  of  dulness  was 
larger  than  it  had  been  previously,  and  pulsation  was  forcible 
and  widespread  in  the  second,  third,  fourth,  and  fifth  inter- 
spaces. The  oedema  on  the  chest  prevented  accurate  observa- 
tions during  her  last  residence,  but  the  area  of  dulness  was 
very  large  on  both  sides  of  the  sternum,  and  pulsation 
was  widespread,  the  whole  prsecordium  heaving  with  each 
systole.  The  maximum  impulse  was  in  the  sixth  interspace, 
well  outside  the  nipple  line,  and  pulsation  was  felt  also 
in  the  interspace  below.  The  liver  showed  an  expansile 
pulsation. 

There  was  a  notable  disproportion  between  the  radial  pulse 
and  the  pulsation  in  the  chest,  the  former  being  soft  and  badly 


NODAL  RHYTHM  145 

sustained,  though  of  moderate  volume,  while  the  latter  was 
violent  and  widespread. 

During  her  numerous  residences  in  hospital  tracings  were 
taken  on  many  occasions.  The  cervical  curves  were  always 
normal  until  March,  1912.  On  March  3  she  complained  of 
severe  pain  in  the  cardiac  region.  The  heart  became  dilated, 
and  the  pulse-rate  rose  to  148.  Tracings  on  the  4th  showed 
an  OrC  interval  of  less  than  0*10  second.  Xext  da^-,  however, 
the  dilatation  had  lessened,  the  pulse  numbered  104  to  120,  and 
the  a-c  interval  exceeded  0*  10  second,  and  thereafter  was  never 
shorter  than  this,  though  it  never  approximated  to  0-20  second. 
Tracings  taken  on  March  10  suggested  the  occurrence  of 
auricular  flutter,  but  those  taken  subsequently  were  of  normal 


Fig.  85. 
Case  6:  The  pulse  is  regular,  and  the  a-c  interval  measures  O'lO  second, 

character.  The  pulse,  too,  was  always  quite  regular,  though 
the  rate  varied  considerably  from,  time  to  time,  and  never  fell 
below  72,  usually  rumiing  between  90  and  100. 

During  her  last  residence  in  hospital  satisfactory  tracings 
were  obtained  on  January  9  and  26,  1913  (Fig.  85).  In  each 
the  pulse  was  regular,  numbering  on  the  first  date  130  and  on 
the  second  145  beats  per  minute.  Venous  congestion  was 
extreme,  and  x  was  absent  in  the  cervical  curve,  v  being 
mingled  with  c.  In  both  tracings  a  was  distinct,  and  preceded 
c  by  less  than  O'lO  second. 

Post-mortem  examination  showed  that  the  visceral  and 
parietal  layers  of  the  pericardium  were  universaUj-  adherent, 
the  layers  being  connected  by  fine,  loose,  fibrous  tissue.  There 
was  a  sHght  loose  fibrosis  in  the  mediastinum.  The  heart  was 
greatly  dilated,  and  the  muscle  was  hj-pertrophied,  the  changes 
being  most  extreme  in  the  left  ventricle.     The  aortic  valve 

10 


146  DISEASES  OF  THE  HEART 

was  markedly  incompetent,  all  the  cusps  being  shortened  and 
shghtly  thickened ;  small  recent  vegetations  were  also  present 
in  the  usual  site.  There  was  a  large  patch  of  atheroma  on  the 
aortic  wall  just  above  the  posterior  cusp.  The  mitral  valve 
admitted  three  fingers.  The  curtains  were  uniformly  thick 
and  stiff,  and  smaU  fresh  vegetations  were  present  on  the 
cusps  and  on  the  chordae  tendinese,  but  the  muscuh  papillares 
were  not  affected.  The  tricuspid  valve  admitted  four  fingers ; 
the  septal  cusp  showed  a  small  acute  ulcer  at  its  free  margin. 
The  pulmonary  valve  was  normal.  The  other  viscera  showed 
evidences  of  gross  venous  congestion,  and  there  was  consider- 
able effusion  into  the  serous  sacs.  Cultures  from  the  spleen 
were  sterile. 

Microscopic  examination  showed  an  extensive  fibrosis  spread- 
ing into  the  tissues  from  the  base  of  the  aortic  and  the  mitral 
valves,  and  several  strands  passing  into  the  a.v.  node.  A 
recent  inflammatory  reaction  was  superadded,  which  also  in- 
volved the  node.  A  similar  state  was  found  at  the  base  of  the 
tricuspid  valve  spreading  backwards  towards  the  node,  and  a 
few  lymphatic  vessels  in  this  situation  were  plugged  with 
leucocytes.  The  cells  were  mainly  lymphocytes,  with  some 
fibroblasts.  The  reaction  was  particularly  marked  around  the 
arterioles,  some  of  which  were  surrounded  by  whorls  of  fibro- 
cellular  tissue,  while  others  were  embedded  in  mononuclear 
collections.  This  was  especially  the  case  in  the  node  and  in 
the  surrounding  auricular  tissue.  The  a.v.  bundle  was  normal 
for  the  greater  part  of  its  course,  but  a  few  strands  infiltrated 
the  lower  part  as  it  passed  behind  the  pars  membranacea. 
The  s.a.  node  was  notably  oedematous,  but  otherwise  normal. 
The  pericardium  overlying  it  was  thickened  and  adherent. 

It  seems  clear,  on  looking  back  upon  the  case,  that  a  sub- 
acute endocarditis  arising  during  the  attack  of  acute  rheuma- 
tism in  December,  1910,  never  really  healed,  and  that  the 
aortic  and  the  tricuspid  disease,  as  weU  as  the  pericarditis, 
were  due  to  a  spread  of  the  infection  from  the  mitral  lesion. 
In  March,  1912,  a  nodule  of  myocardial  inflammation  or  a 
vascular  occlusion  occurred  in  the  vicinity  of  the  a.v.  node, 
occasioning  the  transient  attack  of  nodal  rhythm,  and  perhaps 
the  auricular  flutter  as  weU ;  while  the  permanent  nodal  rhythm 


NODAL  RHYTHM  147 

observed  in  January,  1913,  arose  from  direct  involvement  of 
the  a.v.  node.  At  any  rate,  the  transient  character  of  the 
alterations  in  rhythm  observed  in  March,  1912,  suggests  a 
trivial  or  an  evanescent  cause  for  their  occurrence.  But  it 
was  difficult  to  reahze  during  the  summer  of  1911  that  the 
cardiac  valvuhtis  was  acute.  The  temperature  was  normal, 
and  the  mitral  lesion  did  not  seem  to  be  progressive,  and  a 
sHght  frequency  of  the  pulse  alone  suggested  the  presence  of 
an  acute  cardiac  infection. 

The  tonsils  in  this  patient  were  enlarged,  and  may  perhaps 
have  been  the  source  of  the  recurring  infections.  Their 
removal  subsequent  to  the  attacks  of  chorea  seemed  desirable, 
but  the  operation  was  postponed  in  view  of  the  cerebral  in- 
stabihty,  and  no  further  opportunity  was  afforded  later  on, 
owing  to  the  state  of  her  general  health. 

The  last  case  differs  from  those  which  have  just  been  re- 
ported, in  that  the  patient  was  suffering  from  a  chronic  endo- 
carditis. He  was  a  painter  by  trade,  aged  forty-four,  and  had 
complained  of  cough,  dj'spnoea,  and  dropsy  for  six  months 
before  admission  to  hospital.  The  dropsy  at  this  time  was 
extreme,  and  associated  with  a  large  pleural  effusion,  and  his 
mucous  membranes  were  very  cyanotic.  The  heart  was  con- 
siderably enlarged,  and  double  aortic  and  systolic  mitral 
m.urmurs  were  present.  The  urine  contained  a  consider- 
able quantity  of  albumin.  His  condition  was  extremely 
critical  for  a  few  days,  but  he  ultimately  improved,  though  he 
was  still  breathless  on  trivial  exertion,  and  was  never  able  to 
lie  flat  in  bed. 

Notwithstanding  the  serious  degree  of  cardiac  failure,  the 
pulse-rate  was  never  frequent,  and  usually  numbered  about 
80.  For  some  time  the  pulse  beat  in  couples  and  occasionally 
in  trios,  but  the  rhythm  abruptly  changed  at  varying  intervals 
into  a  regular  beat.  The  cervical  curves  invariably  showed  a 
short  a-c  interval  measuring  0*10  second  (Fig.  86).  His  sub- 
sequent history  is  unknown. 

The  first  six  cases  present  certain  resemblances  and  certain 
differences.  In  all  an  acute  endocarditis  was  present,  which 
affected  the  aortic  valve  alone  in  one  case,  and  the  mitral 


148  DISEASES  OF  THE  HEART 

valve,  and  sometimes  the  aortic  and  tricuspid  valves  as  well, 
in  the  others.  Four  seemed  to  be  due  to  a  rheumatic  infection, 
though  the  organism  was  only  isolated  in  one  case,  and  one  to 
a  streptococcic  infection.  In  five  of  the  cases  a  chronic  endo- 
carditis was  also  present. 

In  all  six  cases  the  a.v.  node  was  involved  in  an  inflammatorj'' 
focus  of  recent  date,  and  in  four  evidences  of  an  old  myocar- 
ditis co-existed.  In  five  the  a.v.  bundle  was  also  slightly  in- 
volved, but  the  lesions  here  were  always  minimal. 

In  all  six  cases  gross  disturbances  of  the  cardiac  functions 
were  observed  during  life.  In  Case  1  a  coupled  rhythm  from 
ventricular  extra-systoles  was  observed  preceding  the  nodal 
rhj^thm ;  in  Case  3  nodal  extra -systoles ;  in  Case  4  ventricular 
extra -systoles.     The  pulse  in  Case  3  was  at  one  time  extremely 


Fig.  86. 
Case  7.  The  pulse  is  regular,  and  the  a-c  interval  measures  0  10  second. 

mobile,  a  bout  of  coughing  quickening  the  rate  from  about 
90  to  about  120  to  130,  the  frequent  rate  persisting  for  a  minute 
or  two  after  the  cough  ceased.  In  Case  2  the  puLse,  which 
was  large  and  collapsing,  became  much  smaller  in  volume  for 
two  days  without  obvious  cause,  and  on  another  occasion  was 
gi'ossly  irregular  for  a  couple  of  hours,  during  which  grave 
symptoms  of  cardiac  exhaustion  were  present.  In  Case  5 
attacks  of  extreme  d^^spnoea  and  faintness  without  obvious 
cause  occurred  on  several  occasions.  In  Case  6  the  pulse-rate 
at  times  varied  very  greatly  in  its  rate,  ranging  from  110  to 
148  in  a  few  hom-s  on  one  occasion,  and  on  another  from  130 
to  180.  In  all  evidences  of  increasing  cardiac  weakness  were 
very  evident,  and  a  regular  pulse-rate,  which  varied  from  110 
to  145,  was  found  to  be  associated  with  a  shortened  a-c  interval 
in  the  cervical  curves. 


NODAL  RHYTHM  149 

The  close  conjunction  of  the  auricular  and  the  ventricular 
contractions  suggests  that  the  stimuli  arose  between  auricle 
and  ventricle.  The  precedence  of  the  auricular  contraction 
suggests  that  they  arose  in  the  vicinity  of  the  a.v.  node.  The 
regularity  of  the  rhythm  suggests  that  they  habitually  arose 
in  one  situation.  In  all  six  cases  the  a.v.  node  was  involved  in 
an  acute  inflammatory  reaction,  such  as  might  render  the  part 
unduly  irritable,  and  so  initiate  stimuli  which  dominated  the 
sinus  influence,  and  set  the  rhj-thm  of  the  heart. 

I  have  been  unable  to  find  any  similar  records  in  the  litera- 
ture,* but  many  comparable  tracings  from  cases  of  paroxysmal 
tachycardia  have  been  pubhshed,  as  well  as  one  electro- 
cardiogram (Lewis).  It  seems  probable  that  paroxysmal 
tachycardia  is  alwaj's  due  to  stimuH  arising  in  some  abnormal 
situation,  as  the  result  of  a  functional  disturbance  enhancing 
the  irritabihty  of  the  part.  A  permanent  change  in  site  of  the 
pacemaker  suggests  that  the  enhanced  irritability  is  due  to  a 
pathological  lesion. 

The  mechanical  interference  with  the  cardiac  work  in  nodal 
rhythm  must  be  considerable,  and  rapidly  produce  cardiac 
failure ;  for  the  closure  of  the  am-iculo -ventricular  valves  during 
auricular  sj'stole  entails  stagnation  of  the  blood  in  the  auricles 
and  great  veins,  a  deficient  supply  of  blood  to  the  ventricles, 
and  relative  ischsemia  of  the  arterial  system. 

The  prognosis  in  cases  of  nodal  rhythm  must  alwaj^s  be 
grave,  for  its  presence  indicates  the  existence  of  an  acute 
myocarditis.  In  the  sixth  case,  however,  its  appearance  was 
at  first  transient,  and  the  patient  lived  for  ten  months  after- 
wards.    The  seventh  patient  left  hospital  in  fair  health. 

REFERENCES. 

CowAX,  KE:!fXEDY,  Patebson,  and  Teacher:  Quart.  Joum.  of  Med.,  1910-11, 

vol.  iv.,  p.  35. 
Cowan,  Fleming,  and  Kennedy:  Lancet,  1912,  vol.  i.,  p.  277. 
Cowan,  Fleminci,  and  Kennedy  :  Trans,  of  the  Internat.  Congress,  London, 

1913. 


*  W.  T.  Ritche  informs  me  that  he  has  recently  obtained  comparable 
electro-cardiogram?,  the  P— R  interval  being  habitually  short.  The  P  wave 
is  positive. 


150  DISEASES  OF  THE  HEART 

It  has  been  known  for  more  than  a  century  that  acute 
rheumatism  is  peculiarly  prone  to  affect  the  pericardium  and 
the  cardiac  valves,  and  is,  indeed,  the  most  common  cause  of 
chronic  valvular  disease ;  but  it  is  only  recently  that  its  special 
action  upon  the  cardiac  muscle  has  been  recognized. 

Acute  rheumatism  sometimes  produces  gross  lesions  in  the 
connective  tissues.  The  occurrence  of  subcutaneous  nodules 
was  first  described  hy  Hillier  in  a  case  of  chorea,  and  Meynet 
and  others  subsequently  recorded  their  association  with  acute 
rheumatism ;  but  the  full  significance  of  their  appearance  was 
only  appreciated  in  1881,  when  Sir  T,  Barlow  and  Warner 
pointed  out  that  the  eruption  of  nodules  was  almost  always 
accompanied  by  acute  endocarditis  of  a  grave  type.  It  had 
aheady  been  recognized  that  in  certain  fatal  cases  of  rheumatic 
endocarditis  the  latter  seemed  insufficient  to  account  for  the 
fatal  issue.  In  some  instances  pericarditis  co-existed,  and 
doubtless  aided  in  the  progress  towards  death;  but  in  others 
it  was  absent,  and  the  chief  clinical  phenomenon  was  progres- 
sive weakness  and  dilatation  of  the  heart;  and  Sturges,  in  his 
Lumleian  Lectures,  maintained  that  the  rheumatic  affection 
of  the  heart  was  not  merely  endocarditis  or  pericarditis,  but 
carditis,  as  all  the  tissues  of  the  organ  were  involved  in  greater 
or  in  less  degree.  It  was  known  that  fatty  and  granular 
changes  were  not  infrequently  present  in  the  cardiac  muscle 
cells  in  the  acute  infections,  and  in  1899  Poynton  demon- 
strated the  essential  lesion,  the  microscopic  submiliary  nodule, 
which,  though  usually  smaller,  is  exactly  comparable  to  the 
lesions  which  occur  in  the  subcutaneous  tissues.  Recent 
observations  have  shown  that  those  lesions  are  not  confined 
to  acute  rheumatism,  but  may  be  found  in  almost  any  infec- 
tion, and  may  occur  in  cases  where  the  valves  and  the  peri- 
cardium are  unaffected,  though  they  are  most  common  in 
cases  where  endocarditis  co-exists.  The  reaction,  too,  is  not 
confined  to  the  myocardium,  but  may  obtain  in  any  or  in  all 
of  the  viscera.  The  microscopic  appearance  of  these  lesions 
has  already  been  described  (p.  20). 

Cellular  infiltrations  are  commonly  present  in  the  tissues  at 
the  bases  of  inflamed  valves,  and  from  the  close  proximity  of 
the  a.v.  system  to  the  mitral,  aortic,  and  tricuspid  valves,  it  is 


NODAL  RHYTHM  151 

often  involved,  and  characteristic  disturbances  of  the  cardiac 
rhythm  make  their  appearance.  The  results  are  of  two  kinds, 
according  to  the  degree  of  the  disturbance,  and  the  system  may 
become  unduly  irritable,  or  may  have  its  functions  completely 
abohshed.  In  the  first  case  extra-systoles  or  nodal  rhj^thm 
may  occur,  in  the  second  heart-block  of  varying  degree. 

The  relations  of  the  a.v.  node  and  bundle  to  the  adjacent 
structures  are  somewhat  perplexing,  for  they  are  rarely  demon- 
strated in  the  dissection  of  the  heart.     The  node  (Fig.  87)  is 
situated  on  the  right  side  of  the  interam-icular  septum  close  to 
the  anterior  edge  of  the  coronary  sinus,  and  immediately  above 
the  insertion  of  the  median  cusp  of  the  tricuspid  valve.     The 
bundle  issuing  from  the  node  at  first  passes  forwards  in  the 
interauricular  septum,   and  then  turns  abruptly  downwards 
through  the  central  fibrous  body  to  reach  the  interventricular 
septum  immediately  behind  the  membranous  septum;  and 
running  forwards  along  its  lower  margin,   divides  into  two 
branches,    which   descend   to   the  right   and   left   ventricles. 
Figs.  88,  89,  90  show  clearly  the  relations  of  the  membranous 
septum.     Fig.  88  is  a  longitudinal  section  of  the  heart,  and 
demonstrates  the  insertion  of  the  median  cusp  of  the  tricuspid 
valve.     The  aortic  cusps  are  rather  above  the  membranous 
septum,  and  the  mitral  valve  is  rather  posterior.     Fig.  89  is 
a  transverse  section  of  the  heart  through  the  septum  looked 
at  from  below,  and  shows  from  another  aspect  the  relation  of 
the  septum  to  the  aortic  and  tricuspid  valves.     Fig.  90  is  also 
a  transverse  section,  but  at  a  rather  higher  level,  and  viewed 
from  above.     It  is  in  practically  the  same  plane  as  the  micro- 
photograph   Fig.  87.      The  orifice   of   the   coronary  sinus   is 
seen  immediately  below  the  Eustachian  valve.     To  its  right  is 
the  interauricular  septum  and  the  central  fibrous  body,  at  the 
lower  margin  of  which  is  a  cusp  of  the  aortic  valve  cut  trans- 
versely, exposing  the  recesses  of  one  of  the  sinuses  of  Valsalva. 
To  its  right  is  a  fragment  of  another  aortic  cusp,  and  to  its 
left  the  membranous  septum  and  the  tricuspid  valve. 

The  relations  of  the  valves  to  the  a.v.  node  and  bundle  are 
weU  shown  in  the  micro-photograph  (Fig.  87).  The  plane  of 
the  section  is  not  quite  horizontal,  but  slopes  downwards  from 
behind.     In  the  uppe    part  of  the  photograph  the  muscular 


^ 


'A 


Aortic  Cusp,  cut  transversely. 

Pulmonary  Artery. 


Membranous  Septum 


Fro.  89. — Transverse  Sectiok  of  the  Heart,  viewed  from  below,  showing 
THE  Relation  of  the  Membranous  Septum  to  the  Valves. 


Tricuspid  Valve. 


Orifice  of  ^^^^^^  ^^^^_ 

Coronary  Stnus.       ^^^  transversely 


Membranous  Septum. 


L.    Vent. 


Fig.  90. — Traissveesb  Section  of  the  Heakt,  viewed  from  above,  showing 
THE  Relation  of  the  Membranous  Septum  to  the  Valves. 


NODAL  RHYTHM 


157 


tissue  of  the  auricle  and  the  insertion  of  the  anterior  cusp  of 
the  mitral  valve  (M)  are  visible,  and  the  section  then  sweeps 
forwards  along  the  lower  part  of  the  membranous  septum, 
terminating  in  the  muscle  of  the  interventricular  septum. 
The  relations  of  the  tricuspid  valve  (T)  to  the  posterior  part, 


X 


Fig.  93. — Micro-Photograph  of  the  a.v.  Node,  SHOwrNG  the  iNFLAJViMATORy 
Reactions  at  the  I^tsertions  of  the  Mitrai  and  Tricuspid  Valves. 
(x5.)     (A.M.  K.) 


and  of  the  aortic  valve  [A]  to  the  anterior  part,  of  the  mem- 
branous septum  are  also  shown,  as  well  as  the  main  bulk  of 
the  a.v.  node,  and  almost  the  whole  length  of  the  a.v.  bundle. 
The  node  is  most  nearly  related  to  the  mitral,  and  the  bundle 
to  the  aortic  and  the  tricuspid  valves. 

Fig.  91  represents  a  similar  section.     The  mitral  valve  in 


158  DISEASES  OF  THE  HEART 

this  case  was  the  site  of  an  acute  endocarditis  engrafted  upon 
a  chronic  lesion,  and  a  dense  fibrosis  can  be  seen  spreading 
from  the  base  of  the  mitral  valve  into  the  adjacent  auricular 
muscle  and  along  the  membranous  septum,  which  is  greatly 
thickened.  There  is  a  well-marked  cellular  infiltration  at  the 
junction  of  the  auricular  muscle  and  the  base  of  the  mitra 
valve  spreading  into  the  node  itself.  In  Fig.  92  the  fibrosis  is 
more  extensive,  and  involves  the  membranous  septum  to  a 
greater  extent.  The  aortic  valve  in  this  case  was  involved  as 
weU  as  the  mitral,  and  the  spread  of  the  fibrosis  from  the  base 
of  the  aortic  valve  into  the  membranous  septum  can  be  clearly 
seen.  In  Eig.  93  a  similar  fibrosis  is  visible  with  a  cellular 
infiltration  spreading  from  the  tricuspid  valve  along  the  septum 
in  the  direction  of  the  a.v.  node. 

The  artery  of  th.Qa.v.  node,  a  branch  of  the  right  coronary 
artery,  is  visible  in  Fig.  87,  and  many  of  the  lesions  which 
affect  the  a.v.  system  are  due  to  interference  with  its  lumen. 


CHAPTER  XI 
CONTRACTILITY 

Contractility  is  the  most  important  individual  function  of 
the  heart,  for  the  maintenance  of  the  circulation  is  dependent 
upon  its  integrity,  and  if  it  fails,  death  ensues.  It  may  be 
measured  by  the  size  of  the  pulse-wave,  for,  as  has  been  aheady 
stated,  the  contraction  of  the  heart  is  always  maximal  irre- 
spective of  the  degree  of  the  stimulus. 

In  extra-systoles  the  size  of  the  pulse-waves  varies  with 
successive  beats  (Fig.  94).  In  this  figure  the  first  six  beats 
are  practically  of  the  same  size,  and  are  succeeded  by  a  small 
premature  wave  c',  a  nodal  extra-systole.  The  small  size  of 
c'  is  not  an  indication  of  defective  contractility.  During 
systole  all  the  functions  of  the  heart  are  in  abeyance,  contrac- 
tility among  the  rest,  and  are  only  gradually  restored  during 
diastole.  If  a  contraction  is  premature,  contractility  is  neces- 
sarily less  restored,  and  as  diastole  is  short,  the  ventricle  is 
imperfectly  filled,  and  the  aortic  blood-pressure  is  relatively 
high,  so  that  the  brachial  wave  is  smaller  than  before.  The 
eighth  (post  extra-systohc)  beat  is  larger  than  normal,  for  as 
diastole  after  an  extra-systole  is  longer  than  usual,  contrac- 
tility is  more  active,  the  ventricular  content  is  larger,  and  the 
aortic  blood-pressure  is  relatively  low.  The  small  size  of  the 
extra-systolic  wave  and  the  large  size  of  the  wave  succeeding 
it  are  merely  the  sequel  to  the  varying  duration  of  diastole. 

The  waves  succeeding  the  post-extra-systolic  beat  vary, 
however,  in  their  size,  though  the  pulse  periods  are  equal,  the 
ninth  and  eleventh  beats  being  smaller  than  the  tenth  and 
twelfth,  and  this  alternation  in  size,  when  the  rhythm  is  regular, 
is  an  indication  of  defective  contractility.  Succeeding  the 
extra-systole  the  diastole  is  prolonged,  and  the  popt-extra- 

159 


160 


DISEASES  OF  THE  HEART 


p^ 


^ 


CONTRACTILITY  161 

systolic  contraction  is  larger  and  more  'prolonged  than  usual. 
In  consequence,  when  the  next  beat  comes  after  an  interval 
of  normal  length,  the  diastole  is  shortened,  and  contractility,  if 
it  is  defective,  is  imperfectly  recovered,  and  systole  is  less 
powerful  and  shorter.  The  shortness  of  systole  entails  pro- 
longation of  diastole,  and  the  next  beat  is  in  consequence 
larger  and  longer ;  and  the  process  is  repeated  indefinitely. 

The  pulsus  alternans  often  continues  for  long  periods  of 
time.  The  pulse  may  be  quite  regular  (Fig.  95),  or  the  small 
wave  may  be  "  delayed  "  (Fig.  96),  but  the  significance  is  the 
same,  for  the  delay  results  because  the  weaker  contractions 
require  a  longer  presphygmic  interval  and  transmission  time; 
the  apical  tracing  is  almost  quite  regular. 

Extra-systoles  must  not  be  confounded  with  the  pulsus 
alternans.  The  distinction  is  easy,  for  an  extra-systolic  beat 
is  always  small  and  premature,  and  is  never  "delayed."  The 
pulsus  alternans  may,  however,  be  closely  simulated  in  Cheyne- 
Stokes  breathing  (Fig.  97).  In  this  tracing  the  size  of  the 
brachial  beats  alternate,  but  the  alternation  is  of  respiratory 
origin,  and  only  obtains  when  the  respirations  increase  in 
frequency  to  such  a  degree  that  they  number  half  the  pulse -rate. 
During  inspiration  the  pulse  is  smaller  than  it  is  during  expira- 
tion, the  pulsus  paradoxus. 

The  pulsus  alternans,  when  continuous,  is  always  of  evil 
import,  and  its  presence,  even  if  only  for  a  few  beats  after  an 
extra-systole,  is  also  serious,  for  in  hearts  of  normal  strength 
the  beats  succeeding  an  extra-systole  do  not  show  the  abnor- 
mahty  (Fig.  77). 


11 


CHAPTER   XII 
CONDUCTIVITY 

Defective  conduction  is  generalty  associated  with  gross 
lesions  in  the  a.v.  bundle.  The  earliest  experiments  were  per- 
formed by  Gaskell,  who  clamped  the  auriculo-ventricular  ring 
in  the  hearts  of  the  tortoise  and  frog,  and  found  that  as  the 
clamp  was  gradual]}^  tightened,  the  interval  between  auricular 
and  ventricular  contractions  gradually  lengthened.  With 
variations  in  the  degree  of  compression  the  ventricle  could  be 
made  to  respond  to  every  second,  third,  fourth  auricular  con- 
traction, or  to  remain  quiescent.  But  in  the  last  case,  after 
a  time,  it  recommenced  beating,  but  independently  of  th& 
auricle  and  with  a  slower  rhythm  of  its  own.  Stanley  Kent 
verified  Gaskell's  conclusions  in  the  rat's  heart,  and  His  and 
many  others  have  demonstrated  the  fact  in  many  mammals 
beyond  any  possible  doubt. 

Chnical  experience  has  now  verified  in  man  the  experimental 
deductions,  and  numerous  cases  are  on  record  where  some 
degree  of  heart-block  was  present  during  hfe,  and  post-mortem 
the  a.v.  bundle  was  affected  by  various  lesions  interfering  in 
greater  or  less  degree  with  its  functional  activity. 

There  is  some  evidence,  however,  which  suggests  that  func- 
tional defect  may  exist  without  gross  disease  of  the  bundle. 
Heart-block  has  been  produced  experimentally  in  many 
ways :  by  the  administration  of  digitahs,  by  the  induction 
of  asphj^xia,  and  hj  vagus  stimulation.  Chnically  James 
Mackenzie  has  found  that  a  pre-existing  defect  (increased 
a-c  interval)  may  be  intensified  by  the  administration  of 
medicinal  doses  of  digitahs  and  by  the  act  of  swallowing ;  and 
Ritchie  and  others  have  noticed  a  similar  result  to  follow  the 
apphcation  of  pressure  upon  the  vagus  nerve  in  the  neck.  In 
full  heart-block,  however,  as  a  rule  the  subcutaneous  injection. 

162 


CONDUCTIVITY  163 

of  atropine  in  doses  sufficient  to  abolish  all  vagus  influence 
fails  to  influence  the  block,  though  in  the  partial  defects 
the  degree  has  been  at  all  events  lessened  (Gibson  and 
Ritchie,  Rihl,  Volhard).  There  is  only  one  case  on  record 
(Hoist  and  Monrad-Krohn)  in  which  the  a.v.  bundle  was  found 
to  be  normal  post-mortem,  though  heart-block  had  been 
demonstrated  during  life.  In  this  instance  both  vagi  nerves 
showed  well-marked  degenerative  changes.* 

Three  grades  of  defective  conductivity  are  recognized : 
1.  Full  Heart-Block. — In  full  heart-block  the  auricular  and 
the  ventricular  contractions  occur  independently  of  each  other. 
In  many  cases  the  auricular  contractions  are  normal  in  rate 


Fig.  98. — Fitll  Heart-Block. 

There  is  complete  dissociation  of  the  auricular  and  the  ventricular  contractions. 
When  these  coincide,  the  cervical  wave  is  large  as  the  auriculo-ventricular 
valve  is  shut,  and  the  auricular  blood  is  thrown  backwards  into  the  jugular 
vein. 

and  rhythm,  and  occur  evidently  in  response  to  sinus  stimuli, 
as  the  rate  alters  on  exertion,  etc.,  as  in  normal  hearts;  while 
the  ventricular  contractions  are  infrequent,  numbering  about 
thirty  per  minute,  and,  though  fairly  legular,  are  the  result  of 
impulses  arising  in  the  ventricle  itself.  But  both  the  auricular 
and  the  ventricular  contractions  may  vary  greatly  in  rate  and 
rhythm  from  time  to  time,  and  a  diagnosis  can  only  be  made 
by  instrumental  methods.  The  dissociation  is  usually  distinct 
in  cervical  curves,  and  often  in  apex  tracings. 

The  cervical  curve  (Fig.  98)  shows  no  regular  relationship 
between  the  a  and  c  waves,  a  now  preceding,  now  following, 
and  now  coinciding  with  the  carotid  beat.  In  the  last  case 
(Beat  3),  the  auricular  wave  is  large,  for  as  the  auricle  is 
contracting  at  the  same  time  as  the  ventricle,  the  auriculo- 
ventricular  valves  are  shut,  and  the  auricular  blood  is,  in 
consequence,  thrown  backwards  into  the  veins.     In  the  apex 

*  W.  T.  Ritcliie  informs  me  that  the  a.v.  tissues  were  normal  in  a  case 
recently  examined  by  him,  though  the  electro-cardiogram  showed  full 
heart-block. 


164  DISEASES  OF  THE  HEART 

tracings  (Fig.  99)  the  a  wave  is  generally  lost  when  aiu'icular 
and  ventricular  systole  coincide,  but  it  is  distinct  during 
ventricular  diastole. 

2.  Partial- Heart- Block. — In  the  lesser  degrees  of  defective  con- 
duction (Fig.  100),  the  ventricular  rhythm  may  be  fairly  regular, 
and  occur  in  response  to  sinus  stimuli,  but  the  interval  between 
the  auricular  and  the  ventricular  contractions  is  increased. 

The  a-c  interval  in  cervical  curves  measures  in  the  normal 
individual  0-15  to  0-20  second,  being  slightly  shorter  when  the 
pulse-rate  is  frequent .  During  the  a-c  interval  five  events 
occur:  (1)  The  contraction  of  the  auricle;  (2)  the  passage  of  the 
stimulus  from  auricle  to  ventricle ;  (3)  the  latent  period  before 
the  ventricle  contracts;  (4)  the  presphygmic  interval;  (5)  the 
transmission  of  the  aortic  wave  to  the  carotid  artery.  The 
average  peiiod  between  the  commencement  of  ventricular 
sj'stole  and  the  appearance  of  the  carotid  wave  is  0-066  second, 
while  the  commencement  of  auricular  contraction  is  practically 
S5mchronous  with  the  appearance  of  the  a  wave  in  the  cervical 
'^urve.  The  presphygmic  interval  and  the  transmission  {time 
(4  and  5)  vary  inversety  with  the  frequency  of  the"'  ventric- 
ular contractions,  and  are  relative^  short  when  diastole  is 
prolonged  (Fig.  80);  auricular  systole,  even  in  cases  of  mitral 
stenosis,  seems  rarely  to  last  for  more  than  0-10  second;  and 
it  seems  certain  that  whenever  the  a-c  interval  measures  more 
than  0-25  second,  the  conduction  of  the  stimulus  from  auricle 
to  ventricle  is  unduly  delayed.  A  possible  fallacy  must  be 
borne  in  mind.  When  the  heart  is  beating  'frequently,  the 
period  of  ventricular  contraction  may  overlap  the  period  of  the 
succeeding  auricular  contraction,  and  a  may  be  merged  in  the 
preceding  v.  |A  similar  overlapping  of  h  and  a  may  also  occur. 
But  these  occurrences  may  be  distinguished  by  an  apical 
tracing,  which  will  show  that  the  a  wave  succeeds  the  appear- 
ance of  the  composite  ^,  or  ^  wave. 

3.  In  the  third  form  a  ventricular  contraction  occasionally 
fails  as  a  result  of  the  defect  (Fig.  101).  With  each  contraction 
of  the  heart  all  its  inherent  functions  'are  in  abeyance  for  the 
time,  'the  stimulus  material  being  exploded,  the  excitabihty 
ost,  'Contractility  abolished,  and  conductivity  minimal  if  'it. 
exists,  though  all  these  functions  are  rapidly  restored  during 


/AWl*kv     IT     .   27    TT     9 

Fig.  100. — Defectr^b  CoNDUCTIO^*j)l. — Pabtial  Heart-Block. 
The  a-c  interval  measures  0-35  second-d  ventricular  contraction  fails. 


[To  face  page  161. 


Fig.  99. — ^Apex  Tracing  in  Full  Heaet-Block. 
The  auricular  and  the  ventricular  contractions  are  fairly  regular. 


■'V..:'i:.'r.:V-.:'i':: 


^ 


B5     I       1-65  I    95      I        15  I   95 


¥ 


Fig.  100. — Defecth'e  Conduotiox. 
The  a-c  interval  measures  0'35  second. 


^^<>^^\^J\]\r^W^ 


Fig.  lOl.— Paktial  Hbaet-Blook. 
Every  third  rentricular  contraction  fails. 


ITo  face  page  164. 


CONDUCTIVITY  165 

diastole.  When  conductivity  is  defective,  frequent  exercise  of 
the  function  entails  further  defect.  In  Fig.  101  conductivity 
is;S0  defective  that  even  after  a  ventricular  rest  of  1-35  seconds 
the  a-c  interval  measures  0-30  second.  The  succeeding 
auricular  contraction  occurs  0-55  second  later,  and  the  shorter 
rest  necessitates  a  longer  period  (0-40  second)  for  the  trans- 
mission of  the  stimulus  ;  and  when  another  auricular  contraction 
occurs  0-35  second  later,  the  stimulus  fails  to  pass,  and  a 
ventricular  contraction  is  missed.  But  the  longer  rest  which 
thus  ensues  improves  conductivity,  and  ventricular  con- 
traction succeeds  the  ensuing  auricular  contraction  by  a  shorter 
interval,  [and  the  process  is  repeated  indefinitely.  The  radial 
pulse  may  be  almost  regular  in  these  cases  if  every  second 
auricular  contraction  fails ;  or  every  third  or  fourth,  ven- 
tricular beat  alone  maj^  be  missed. 

The  chronic  'forms  of  full  heart-block  are  not  necessarily 
associated  with  any  definite  signs  of  cardiac  distress,  and  Sir 
WiUiam  Gairdner,*  for  example,  who  died  at  the  age  of  eighty- 
two,  enjoyed  fair  health  for  the  last  four  years  of  his  life, 
though  there  was  complete  dissociation  for  all  this  period.  In 
the  majority  of  cases,  however,  some  degree  of  cardiac  in- 
sufficiency is  present — weakness,  shortness  of  breath  upon 
exertion,  etc. — though  these  are  to  be  related  rather  to  the 
causes  which  produced  the  block  than  to  the  block  itself. 
The  heart  itself  is  rarely  normal,  valvular  flaws  are  common, 
and  the  musculature  is  apt  to  be  affected  diffusely  by  lesions 
similar  to  those  which  have  involved  the  a. v.  bundle. 

The  pulse  in  these  circumstances  is  uniformly  infrequent, 
numbering  [about  30  per  minute,  and  is  generally  regular 
in  rhythm.  The  rate  may  vary  slightly  from  time  to  time, 
but  it  is  little  influenced  by  emotion,  exercise,  fever,  etc.,  which 
produce  [notable  effects  upon  a  normal  heart.  A  pulse-rate 
of  under  40  per  minute  of  itself  suggests  heart-block,  as  the 
other  conditions  which  may  produce  so  slow  a  rate  are  much 
more  rare,  and  I  have  only  observed  it  twice,  once  in  jaundice 
and  once  in  cerebral  tumour,  in  both  of  which  the  rate  was  39, 

*  G.  A.  Gibson  and  W.  T.  Ritchie:  Edin.  Med.  Joum.  N.S.,  vol.  ii.. 
pp.,  315,  507;  Lancet,  1909,  vol.  i.,  p.  533. 


166  DISEASES  OF  THE  HEART 

with  normal  cervical  curves.  In  the  first  case  the  pulse  rose  to 
normal  rates  when  the  jaundice  passed  away,  and  a  similar 
event  occurred  in  the  latter  after  a  decompression  operation. 
In  a  patient  w^ho  was  suffering  from  tobacco  intoxication  the 
pulse  numbered  40,  and  I  have  pulse-rates  of  46  after  pneu- 
monia and  48  after  influenza,  with  normal  curves. 

The  evidences  of  auricular  action  in  the  jugular  veins  may 
be  visible,  as  was  described  by  Stokes :  "A  new  symptom 
appeared,  namely,  a  remarkable  pulsation  in  the  right  jugular 
vein.  This  was  most  evident  when  the  patient  lay  down. 
The  number  of  the  reflex  pulsations  was  difficult  to  be 
estabhshed,  but  the}^  were  more  than  double  the  number  of 
the  manifest  ventricular  contractions.  About  every  third 
pulsation  was  strong  and  sudden,  and  could  be  seen  at  a 
distance;  the  remaining  waves  Were  much  less  distinct,  and 
some  very  minor  ones  could  be  perceived."* 

Auscultation  furnishes  another  sign.  If  the  pulse  is  regular 
and  a  mitral  systohc  murmur  co-exists,  regurgitation  into  the 
auricle  wiU  cease  when  ventricular  and  auricular  contraction 
coincide,  and  the  murmur  will,  in  consequence,  disappear  or 
weaken  {cf.  Fig.  98).  The  murmur  of  mitral  reflux,  of  course, 
varies  in  its  intensity  and  duration  in  cases  of  auricular 
fibrillation,  according  to  the  duration  of  diastole  and  the  degree 
of  filling  of  the  ventricle ;  but  it  does  not  alter  in  cases  with 
regular  ventricular  contractions  unless  auricular  contractions 
coincide  with  the  ventricular. 

In  some  cases  the  auricular  contractions  may  produce 
audible  (single)  sounds,  but  this  is  hx  no  means  constant,  even 
in  cases  where  the  auricles  have  been  sho^\Ti  to  contract 
rhythmically,  and  not  to  be  in  flutter  or  in  fibrillation.  Person- 
ally I  have  never  heard  them. 

A  diagnosis  can  be  readily  made  with  instrumental  aid,  the 
dissociation  being  shown  in  the  cervical  or  the  apex  curves. 

In  full  heart-block  a  very  striking  series  of  symptoms,  the 
Stokes-Adams  syndrome,  is  not  infrequently  observed.  It  may 
occur  at  any  period,  but  is  most  common  in  the  early  stages 

*  "  Diseases  of  the  Heart,"  1854,  p.  315.  Dublin  Quart.  Journ.  of  Med.  Sci., 
1846,  vol.  ii.,  p.  73. 


CONDUCTIVITY  167 

during  the  development  of  the  fuU  block,  and  it  often  dis- 
appears with  its  estabhshment,  though  in  exceptional  cases 
it  has  recurred  later  on.     A  typical  example  is  recorded  below. 

The  patient,  an  engineer,  aged  fifty-seven,  had  been  employed 
in  tropical  chmates  for  some  thirty  years .  His  health  had  been 
good  while  abroad,  save  for  occasional  attacks  of  ague.  He  had 
suffered  from  gonorrhoea  twenty  years  before,  accompanied  by 
a  sore  which  was  not  considered  to  be  syphilitic,  and  was  not 
followed  by  any  secondary  symptoms.  Four  years  before  his 
illness,  however,  he  began  to  "  feel  the  tropics,"  and  two  years 
later  he  came  home  on  a  year's  furlough.  He  did  not  return  to 
his  work,  as  he  felt  that  he  was  not  fit  for  it,  though  he  had  no 
definite  symptoms  save  on  one  occasion  slight  swelling  of  the 
feet,  which  disappeared  in  a  few  days . 

The  symptoms  for  which  he  came  under  observation  com- 
menced quite  suddenly  three  months  before,  when  he  was 
living  in  Stirhng.  He  was  going  to  the  Perth  race-meeting  and 
was  late  in  rising,  so  that  his  breakfast  was  hurried.  When  he 
was  walking  smartly  to  the  railway-station,  he  suddenly  felt 
faint  and  had  to  clutch  hold  of  some  raihngs  to  prevent  himself 
from  falling ;  but  the  f aintness  passed  away  in  a  few  moments . 
When  walking  to  the  luncheon-stand  at  Perth  in  the  afternoon 
he  again  felt  faint,  and  on  this  occasion  lost  consciousness,  and 
feU  to  the  ground,  but  he  rapidly  recovered.  He  attributed  the 
seizures  to  starvation,  and  after  lunch  he  felt  better  and  stayed 
on  at  the  races .  He  slept  well  at  night,  but  next  morning,  while 
sitting  quieth"  in  his  rooms,  he  had  some  thirty  seizures  of  a 
similar  kind. 

These  attacks  have  continued  at  irregular  intervals  ever 
since.  He  was  sometimes  free  from  them  for  as  long  as  a 
week,  but  sometimes  they  recurred  several  days  in  succession. 
On  one  occasion  he  fell  down  and  cut  his  face.  Two  weeks 
before  admission  the  attacks  became  more  numerous  and 
more  severe.  For  hours  at  a  time,  the}^  recurred  frequently, 
and  lasted  for  longer  periods,  and  were  associated  with 
twitchings  of  the  muscles,  and  in  consequence  he  felt  weak 
and  exhausted.  The}-  were  generally  preceded  by  a  dull 
pain  in  the  upper  part  of  the  right  chest. 

For  three  days  after  his  admission  to  hospital  the  attacks 


168  DISEASES  OF  THE  HEART 

did  not  recur,  but  they  recommenced  next  day  at  7  a.m.,  and 
continued  all  daj^  at  short  intervals ;  some  200  occurred  in 
the  twenty-four  hours.  Next  day  he  had  seven  attacks,  and 
on  the  succeeding  day  thirteen,  but  there  were  only_^ eleven  m 
the  next  eight  days,  and  about  twenty  on  the  last  day  of  his 
residence.  They  subsequently  continued  to  be  infrequent  and 
of  short  duration. 

Manyjattacks  were  observed.  They  were  all  similar  in  type. 
The  apex  impulse  was  large  and  prominent,  and  the  first  thing 
that  was  noticed  was  the  cessation  of  the  apex  impulse  and 
the  radial  pulse.  Simultaneously  he  said  that  he  felt  giddy 
and  that  a  fit  was  impending,  his  countenance  became  white 
and  anxious,  and  he  moved  his  arms  restlessly  and  tried  to 
catch  hold  of  the  bedstead.  In  two  or  three  seconds  he 
became  unconscious,  and  a  slight  tonic  spasm,  which  some- 
times seemed  purposeful,  ensued ;  and  this  was  followed,  if  the 
ventricular  asystole  continued,  by  clonic  spasms,  which  com- 
menced in  the  face  and  spread  to  the  arms  and  sometimes  also 
to  the  legs.  In  a  few  seconds  the  face  suddenly  fiushed,  and 
the  apex  impulse  and  radial  pulse  reappeared ;  he  straightened 
his  head,  and  consciousness  returned. 

Convulsions  did  not  occur  in  every  attack.  Many  were  of 
very  short  duration,  and  only  lasted  for  five  or  six  seconds 
(Fig.  102),  in  which  case  no  convulsion  ensued,  but  others 
lasted  for  ten  to  fifteen  seconds,  and  were  then  accompanied 
by  muscular  movements.  These,  however,  even  when  general, 
were  never  gross,  and  incontinence  never  occurred.  Recovery 
after  jthe  attacks  was  rapid  and  complete,  but  he  said  that  he 
felt  tired  and  exhausted. 

He  was  a  tall,  well-developed  man,  but  his  muscles  were 
small  and  soft,' and  the  subcutaneous  tissue  scanty.  His  hair 
was  white,  and  he  looked  older  than  his  years,  and  somewhat 
weakly.  There  was  no  oedema,  but  the  liver  seemed  to  be 
enlarged.  There  was  a  sHght  bronchial  catarrh,  and  a  trace 
of  albumin  in  the  urine. 

The  apex  impulse  was  situated  in  the  fifth  interspace, 
4|  inches  from  mid-sternum,  and  was  punctate  and  prominent 
and  well-sustained.  The  area  of  cardiac  dulness  measured 
4|  inches  transversely.     The  cardiac  sounds  were  faint;  the 


Fig,  102. — Brachial  Curve  from  a  Case  oe  Full  Heart-Blook. 
The  auricular  contractions  are  distinctly  visible. 


CONDUCTIVITY  169 

second  aortic  sound  was  intoned  and  ringing ;  the  first  sound 
at  the  apex  was  prolonged  and  impure,  and  on  some  days  suc- 
ceeded by  a  rather  harsh  murmur.  The  auricular  contractions 
were  never  audible.  The  arteries  generally  were  thickened, 
hard,  and  tortuous.  The  pulse  was  fuU,  and  the  blood- 
pressure^measured  145 — llOmm.Hg. 

The  pulse  as  a  rule  was  fairly  regular  and  infrequent, 
usually  running]  about  28  to  32  per  minute  (Fig.  99),  and 
at  these  times  attacks  did  not  occur.  On  other  occasions 
it  was  extremely  irregular  (Fig.  102),  and  a  pause  of  several 
seconds  might  appear  between  successive  beats,  or  the  pulse- 
rate  [might  increase,  and  number  even  56  per  minute,  a  rate 
which  was  observed  on  two  or  three  occasions. 

^Cervical  curves  were  not  obtainable  as  the  clavicles  were 
deformed  and  covered  the  jugular  bulb,  but  the  apex  and 
brachial  tracings  showed  plainly  the  dissociation  of  the 
auricular  and  the  ventricular  contractions,  the  auricular  beats 
being  fairly  regular  and  numbering  about  66  per  minute,  quite 
irrespective  of  the  rate  or  the  rhythm  of  the  ventricles. 

The  attacks  may  be  of  varying  nature  and  duration.  In  the 
shorter  seiziKes  they  are  simple  syncopes,  while  in  ,those  of 
longer  duration  convulsions  often  supervene  both  of  the  tonic 
and  the  clonic  kind.  Recurring  attacks  at  short  intervals 
may  persist  for  hours  on  end,  or  even  for  a  day  or  two,  and 
while  in  some  cases  they  are  isolated  events,  they  may  return 
after  intervals  of  weeks  or  months  for  two  years  (Sir  W. 
Gairdner),  or,  for  fourteen  years,  as  in  one  of  Mackenzie's  cases. 

It  must  be  clearly  understood  that  heart-block  and  the 
Stokes-Adams  syndrome,  though  frequently  associated,  are 
not  synonymous.  Many  cases  of  full  heart-block  without  the 
syndrome  have  been  recorded,  and  the  Jsyndrome  may  occur 
without  block.  In  heart-block  the  pulse  is  quite  regular,  and 
numbers  about  30  per  minute.  In  the  syndrome  the  pulse 
is  irregular  and  ver^'  infrequent,  numbering  5  to  20  per 
minute,  and  long  intervals  of  [many  seconds'  length  may 
occur  between  beats.  jThis  latter  featm-e  is  the  essential  point. 
Kussmaul  and  Tenner  showed  that  cerebral  anaemia,  induced 
by  hgature  or  compression  of  the  carotid  arteries,  produced 


170  DISEASES  OF  THE  HEART 

loss  of  consciousness,  and,  if  continued,  convulsion;  and 
observations  of  many  attacks  by  numerous  observers  have 
made  it  clear  that  the  ventricular  contractions  cease  prior 
to  the  onset  of  the  cerebral  symptoms ;  and  that  this  is  the 
cause  of  the  attacks. 

Sir  William  Osier  has  reported  two  cases  of  the  syndrome 
in  which  heart-block  seems  definitely  excluded.  In  one  the 
patient  suffered  from  tubercular  disease  of  the  first  and 
second  cervical  vertebrae,  and  had  on  several  occasions  attacks 
of  syncope  and  slow  pulse.  Another  patient  suffered  from  a 
sarcoma  of  the  medulla,  and  experienced  similar  seizures.* 

The  cause  of  the  cessation  of  the  ventricular  contractions 
is  in  all  probability  the  lesion  which  produces  the  block. 
Gaskell  pointed  out  that  if  a  cut  was  made  close  against  the 
ventricle  in  the  auriculo-ventricular  groove,  the  ventricle  beats 
rapidly  for  a  time,  and  then  gradually  slows  until  at  last  it 
stands  still ;  and  after  a  variable  period  it  begins  to  beat  again, 
at  first  very  slowly,  but  ultimately  more  frequently  and 
regularly.  If,  on  the  other  hand,  the  junction  is  clamped  very 
slowly,  the  ventricle  ceases  to  beat  without  any  initial  increase 
in  its  rate  of  contraction.  A  sudden  stimulus  produces  an 
initial  rhythm  of  excitation ;  a  slowly  applied  stimulus  merely 
abohshes  the  function ;  while  in  time,  after  either,  the  inherent 
rhythmicity  of  the  ventricle  comes  into  play,  and  the  ventricular 
contractions  develop  with  their  own  special  rate. 

The  lesions  which  have  been  found  in  heart- olock  in  the 
a.v.  tissues  are  of  various  kinds.  In  some  cases  they  are  of 
acute  character,  abscess,  arterial  occlusion,  etc. ;  in  others,  they 
are  chronic,  a  dystrophic  fibrosis,  tumour,  etc.,  and  acute  or 
chronic  inflammatory  reactions  may  occur  in  their  vicinity. 

In  some  cases,  then,  the  lesion  may  irritate  and  provoke  a 
frequent  ventricular  rate,  and  in  other  cases  inhibit  the 
ventricular  contractions  for  a  time.  And  fresh  lesions  or  an 
exacerbation  of  the  secondary  inflammatory  reaction  may 
repeat  for  an  indefinite  period  the  symptoms  which  ensued 
at  the  onset.  An  old  scar  is  unirritating,  'and  the  chronic 
form  of  heart-block  with  a  regular  infrequent  pulse  is  its 
accompaniment . 

*  Article  in  AUbutt's  System,  1909,  vol.  vi.,  p.  130. 


CONDUCTIVITY  171 

The  dangerous  period  of  heart-block  is  thus  the  initial  stage, 
the  period  when  lesions  are  forming  in  the  a.v.  tissues.  When 
once  the  block  is  full  and  the  scar  contracted,  the  danger  of 
ventricular  asystole  from  this  cause  is  past. 

In  full  heart-block  the  ventricles  seem  to  be  outwith  the 
influence  of  external  stimuli,  such  as  vagus  pressure  or  the 
injection  of  atropine,  though  these  may  a£Pect  the  rate  of  the 
auricular  contractions,  a  fact  which  harmonizes  with  the 
current  conception  that  the  a.v.  bundle  is  the  onlj  channel 
through  which  impulses  of  any  kind  travel  from  auricle  to 
ventricle.  In  partial  block,  however,  the  administration  of 
atropine  may  lessen  the  degree  of  block,  and  vagus  pressure 
may  increase  it,  though  as  a  rule  such  procedures  have  httle 
effect. 

The  Auricular  Contractions  in  Heart-Block. — The  auricular 
action  in  heart-block  is  not  always  normal,  for  the  auricles  may 
be  fibrillating  (Mackenzie,  Lewis),  or  in  flutter  (Ritchie);  but 
these  seem  to  occur  only  in  exceptional  cases.  The  actual 
condition  of  the  auricles  is  apparently  immaterial  with  regard 
to  the  prognosis ;  the  important  factor  is  the  rate  of  the  ven- 
tricular contractions.  Ritchie's  patient,  with  flutter  and  block, 
is  stiU  ahve  and  in  fair  health,  though  the  condition  was  recog- 
nized more  than  seven  years  ago ;  and  one  of  Mackenzie's  cases 
of  fibrillation  and  block  was  working  regularly  four  years  after 
the  condition  was  recognized. 

Cases  with  partial  heart-block,  too,  have  no  necessary  incon- 
venience from  their  disability.  In  some  instances  the  block 
may  become  complete  for  a  time,  the  pulse  may  run  at  a  very 
slow  rate,  and  the  Stokes-Adams  syndrome  may  ensue,  but 
in  the  majority  they  are  recognized  on  critical  examination  of 
an  irregular  pulse  or  on  routine  examination  of  a  faihng 
heart.  Symptoms  of  cardiac  insufficiency  may  or  may  not  be 
apparent,  but  if  present  are  only  in  small  degree  the  result  of 
the  block.  Palpitation  is  frequently  experienced  by  these 
patients . 

The  lesions  which  are  found  in  Ithe  a.v.  tissues  on  post- 
mortem examination  are  varied.  The  following  hst  is  derived 
from  those  of  Hirschfelder  and  Lewis  :  Gumma,  7 ;  calcification, 
7;  fibrosis,  11;  tumour,  2;  anaemic  infarction,  2;  round-celled 


172  DISEASES  OF  THE  HEART 

infiltration,  4;  mural  ulceration,  1;  fatty  degeneration,  1; 
arterio-sclerosis  of  a.v.  arterj',  1. 

Tlie  majority  of  these  cases  are  thus  chronic  in  their  nature, 
but  heart-block  may  occur  in  acute  disease.  In  1905  James 
Mackenzie  repoited  the  transient  occurrence  of  the  milder 
grades  of  block  in  patients  who  were  suffering  from  acute 
rheumatism  and  influenza,  and  since  then  several  cases  of  full 
heart-block,  -vvith  post-mortem  examinations,  have  been  recorded 
(gonococcic  endocarditis,  ulcerative  endocarditis,  diphtheria, 
acute  rheumatism,  quickly  followed  b}-  enteric  fever).  Clinic- 
ally it  has  been  observed,  either  complete  or  partial,  in  pneu- 
monia, scarlatina,  and  enteric  fever. 

Transient  defects  are  not  uncommon  in  acute  rheumatic 
endocarditis,  and  I  have  observed  five  examples.  In  one  case 
the  defect  persisted  for  nearty  four  weeks ;  in  another  it  dis- 
appeared after  six  days,  recurred  three  days  later,  and  again 
lasted  for  six  days .  In  none  of  these  cases  was  there  complete 
block,  but  in  one  the  ventricles  only  responded  to  every  second 
auricular  contraction.  All  the  cases  made  good  recoveries, 
and  in  one  alone  was  the  ultimate  valvular  lesion  severe. 

In  exceptional  cases  the  Stokes-Adams  syndrome  may  occur. 
My  colleague,  W.  D.  Macfarlane,  observed  this  in  a  case  of 
acutCj  rheumatic  endocarditis,  in  which  the  pulse-rate  fell 
as  low  as  15  per  minute,  with  occasional  long  intervals 
between  the  beats.  On  these  occasions  the  patient  lost  con- 
sciousness, and  the  muscles  of  the  face  and  arms  twitched. 
The  convulsions  recurred  for  two  or  tlu'ee  weeks,  but  recovery 
ensued  after  a  tedious  convalescence.  He  lived  for  more  than 
ten  years,  and  eventually  died  from  chi'onic  valvular  disease. 

The  prognosis  in  heart-block  is  based  upon  two  factors,  the 
degree  of  the  block  and  its  cause.  In  a  general  way  the  prog- 
nosis is  grave,  for  |its  presence,  whether  partial  or  complete,  is 
an  indication  of  serious  mj'^ocardial  disease.  The  presence  of 
valvular  lesions  is  probably  of  little  moment.  The  a.v.  tissues 
are  most  frequently  affected  in  valvular  disease,  but  this  is 
owing  to  their  close  proximit}^  to  the  valves,  and  the  myo- 
carditis is  not  necessarily  mdespread.  If  the  lesion  is  due  to 
an  acute  process,  it  may  subside  (acute  rheumatism)  or  progress 
(mahgnant  endocarditis);  if  due  to  a  chronic  arterial  change,  it 


CONDUCTIVITY  173 

wiU  tend  steadily  to  increase.  A  syphilitic  lesion  may  resolve 
under  treatment  (Osier).  The  presence  or  absence  of  signs  of 
myocardial  insufficiency  is  necessarily  important. 

Chronic  full  heart-block  is  not  incompatible  with  many 
years  of  fair  health.  A  partial  block  may  become  complete 
or  may  pass  away.  And  as  the  danger  of  the  cessation  of 
ventricular  contraction  occurs  in  cases  of  partial  block,  and 
in  full  block  about  the  period  of  its  development,  the  lower 
grades  are  probably  more  important  than  the  complete  form. 
Here  again,  as  usual,  the  experience  of  the  individual  patient 
is  important,  and  a  low  rate  of  the  pulse  or  the  occurrence  of 
even  trivial  syncope  or  convulsion  renders  the  immediate 
prognosis  extremely  grave. 

Chronic  full  heart-block  demands  no  special  treatment  beyond 
that  indicated  by  the  general  symptoms. 

In  partial  block  'complete  rest  is  certainly  indicated,  for 
exertion  is  bound  to  increase  the  work  of  the  heart,  and  so  to 
increase  in  some  measure  the  inflammatory  reaction  and  the 
ultimate  scar.  The  administration  of  digitalis  is  contra- 
indicated,  for  it  tends  to  exaggerate  defective  conductivity, 
and  vagus  pressure  has  a  similar  effect.  'In  certain  cases  the 
administration  of  atropine  {-xlrn  ^^  tV  grain)  has  lessened  or 
abohshed  the  block  and  so  increased  the  number  of  the  iven- 
tricular  contractions,  and  it  should  certainly  be  given  if  the 
ventricular  rate  becomes  infrequent.  In  most  cases  it  has  no 
action  of  this  kind.  The  diffusible  stimulants — strychnine, 
hot  fomentations  to  the  prsecordia,  etc. — are  most  likely  to  be 
useful. 

'In  full  block,  digitahs,  atropine,  and  vagus  pressure  have  no 
influence  upon  the  rate  of  the  ventricular  contractions . 


CHAPTER  XIII 
TONICITY 

The  recurring  contractions  of  the  heart  interfere  with  the 
recognition  of  the  tone  of  the  cardiac  muscle  at  any  particular 
moment,  for  it  is  evident  that  the  degree  of  diastoHc  relaxation 
is  dependent  upon  the  duration  of  diastole  as  well  as  upon  the 
tone  of  the  muscle.  But  it  has  been  clearly  shown  that  the 
heart  possesses  this  quahty,  for  the  application  of  drugs,  such 
as  sodium  hydrate,  to  the  beating  heart,  is  followed  by  less 
and  less  complete  relaxation,  until  finally  the  heart  remains 
in  a  condition  of  systolic  standstill.  The  apphcation  of  other 
drugs,  such  as  lactic  acid,  moreover,  produces  atony,  and  the 
contractions  become  more  and  more  feeble  until  the  heart 
stands  still  in  complete  relaxation. 

When  tone  is  defective,  the  heart  becomes  dilated,  the 
apical  pulsation  is  displaced  and  diffuse,  the  area  of  cardiac 
dulness  is  increased  transversely,  and  evidences  of  general 
venous  engorgement  make  their  appearance.  The  mitral  or 
the  tricuspid  valve  may  become  incompetent. 


174 


CHAPTER  XIV 
COUPLED  RHYTHMS 

In  pulsus  alternans  a  large  and  a  small  pulse-beat  alternate, 
and  a  somewhat  similar  allorrhythmia  obtains  in  coupled 
rhythm.  There  is,  however,  an  essential  difference,  for  in 
pulsus  alternans  the  interval  between  the  smaller  beat  and 
that  preceding  it  is  longer  than,  if  not  equal  to,  the  interval 
between  the  smaller  beat  and  that  which  succeeds  it  (Figs.  95 
and  96) ;  while  in  coupled  rhythm  the  period  between  the  small 
beat  and  the  succeeding  larger  wave  is  always  the  longer 
(Fig.  103). 

Coupled  rhythm  may  be  due  to  various  causes.  The  most 
common  form  is  the  result  of  a  regularly  recurring  ventricular 
extra-systole,  or,  less  frequently,  a  nodal  extra-systole.  It  may 
obtain  in  nodal  rhj^thm,  in  auricular  fibrillation,  and  in  the 
various  degrees  of  heart-block.  In  some  instances  both  auricle 
and  ventricle  share  in  the  coupling ;  in  others  the  ventricles 
alone  are  involved. 

A  coupled  rhythm  may  occur  in  partial  heart-block.  This  is 
shown  in  Fig.  104,  which  was  obtained  from  a  patient  suffering 
with  acute  rheumatism,  in  whom  defective  conduction  obtained 
for  a  month.  In  the  tracing  the  a-c  interval  is  always  pro- 
longed, the  first  auricular  contraction  being  followed  by  the 
carotid  wave  after  an  interval  of  0-30  second.  The  second  a-c 
interval  measures  0-35  second,  and  with  the  third  auricular 
contraction  the  stimulus  fails  to  pass.  During  the  lengthened 
rest  which  ensues  in  consequence,  conductivity  is  restored,  so 
that  the  fourth  auricular  contraction  is  followed  by  a  ven- 
tricular contraction  after  an  interval  of  again  0-30  second; 
but  with  the  next  beat,  as  the  period  of  rest  is  shortened,  the 
a-c  interval  is  longer  (0-40  second),  and  the  sixth  auricular  beat 
again  fails  to  produce  a  ventricular  response. 

175 


176 


DISEASES  OF  THE  HEART 


The  coupled  rhythm  wliich  occurs  in  auricular  fibrillation 

resembles  somewhat  closely  those  forms  in  which  it  is  due  to 

a  regularly  recurring  extra-systole.     As  will  be  seen  (p.  213), 

the  ventricular  beats  in  auricular  fibrilla- 

3  tion   are  in   response  to   impulses   which 

o  descend  from  the  fibrillating  auricle,  and 

%         are  therefore  comparable  to  phj^siological 

g  contractions  of  the  ventricle,  and  electro- 

g  cardiographic   investigations   have   shown 

1^  that  the  smaller  beat  of  the  couple  in  these 

fc,  cases   is    due   to  an  intrinsic  ventricular 

o 

jH  contraction,    or,    in    other    words,    to    a 

%  ventricular  extra-sj^stole. 


-i 


-i 


-C 


-r 


H 


Henschen*  pointed  out  that  coupled 
rhythm  occurs  most  frequently  in  cases  of 
mitral  disease  with  a  feeble  heart,  and  a 
pulse-rate  which  is  infrequent  from  full 
doses  of  digitalis  ;  and,  arguing  from  radial 
tracings  alone,  suggested  that  in  these 
cases,  on  account  of  the  prolonged  diastole 
produced  bj^  the  drug,  the  auricles  were 
incompletely  emptied  at  their  regular  sys- 
tole. With  the  succeeding  ventricular 
contraction  the  reflux  from  the  ventricle 
still  further  distended  the  left  auricle,  and 
the  excessive  pressure  which  resulted  in- 
cited the  auricle  to  contract  prematurely. 
As  diastole  was  short,  the  ventricle  was 
imperfectly  filled,  and  the  aortic  wave  was  in 
consequence  small.  Following  the  extra- 
systole,  the  auricular  excitability  was  so  far 
reduced  that  a  complete  distension  of  its 
cavity  was  required  to  provoke  a  new  con- 
traction, and  the  succeeding  diastole  was  in 
consequence  prolonged,  and  more  or  less  compensatory.  But 
while  this  theory  is  extremely  plausible,  it  is  only  applicable 
to  cases  in  which  the  second  beat  of  each  couple  is  a  regularly 
*  Mitteil.  a.  d.  me:l.  Klinih  zu  Upsala,  1898,  i. 


COUPLED  RHYTHMS 


177 


recurring  auricular  extra-systole,  an  undoubted  example  of 
which  has  not  yet  been  recorded,  the  large  majority  of  cases 
being  due  to  ventricular  extra-systoles. 

The  question  is  discussed  at  length  in  the  Quarterly  Journal 
of  Medicine  by  Ritchie  and  myself,*  and  we  have  suggested 
that  "  whenever  an  enfeebled  heart  is  unduly  irritable  in  an 
abnormal  site,  any  excessive  rise  of  intracardiac  pressure  may 
produce  a  regularly  recurring  premature  systole  which  origi- 
nates at  the  irritable  area." 

Extra-systoles  may  arise  in  any  part  of  the  heart,  and  are 
probably  the  result  of  a  local  hyper-excitability  produced  in 
some  cases  by  local  myocardial  lesions,  and  in  others  by 
functional  disturbances .     Experimental  researches  have  demon 


/Au/i*+ij^  jr  .  27"n-    9 


Fig.   104. — Coupled  Pv,hythm:,  due  to  Partial  Heart- Block,  every  Third 
Ventricular  Contraction  failing. 


strated  that  extra-systoles  may  be  induced  by  constriction  of 
the  aorta  or  the  pulmonary  artery,  or  by  reflex  stimulation  of 
the  vasomotor  centres,  which  produces  a  rise  in  the  intra- 
cardiac pressure ;  and  a  rise  will  also  certainly  accompany  the 
synchronous  contraction  of  auricle  and  ventricle,  or  any  undue 
prolongation  of  diastole. 

Synchronous  contraction  of  auricle  and  ventricle  is  often 
followed  by  a  premature  auricular  or  ventricular  contrac- 
tion. In  Fig.  105  the  fourth  ventricular  contraction  occurs 
sjaichronously  with  a  regular  auricular  contraction.  As  a  result 
the  auricle  is  unable  to  empty  its  contents  into  the  ventricle 
and  at  the  end  of  its  diastole  is  notably  engorged.  The  intra- 
auricular  pressure  is  rapidly  increased  by  the  influx  of  blood 


*  1910-11,  vol.  iv.,  p.  55. 


12 


178 


DISEASES  OF  THE  HEART 


from  the  congested  veins,  and  the  fifth  auricular  contraction  is 
in  consequence  premature, 

A  similar  coincidence  is  sometimes  observed  in  heart-block. 
In  Fig.  106  a  partial  heart-block  is  present,  and  occasional 
ventricular  contractions  drop  out.     Reference  to  the  accom- 


6S-      I  'n-^Fi. 


'(>S        I  -^     I      bS       I      '65-       I -45    r~^«S-       I      'fcs        I       ••>         I     -65     \^^-:'^^~ 

acvac   vac  vcg  ^a  c  vMac  v  ca^o-c  v    a^c  \r  gc  \y  ac    v 

Fig.  105. 
The  ventricular  extra-systoles  are  followed  by  premature  auricular  contractions. 

panying  diagram  shows  that  the  auricular  rhythm  is  also 
irregular,  the  a-a  periods  varying  between  0-50  to  0-70  second. 
The  sphygmic  periods  are  plotted  out  in  the  diagram,  and  it  is 
evident  that  the  shorter  a-a  periods  succeed  synchronous  con- 
traction of  auricle  and  ventricle,  the  periods  being  shorter, 


E 


3^ 


•S5 


•65 


•6S 


^ 


::^ 


nK 


E 


xs 


e: 


s 


a.  e   4 


aeok      ca        a,    c    a. 


a.  c     oi 


a  c 


<x.  tf    a.      C  a 


Ok.  ce 


K 


Fig.  lOG. — Partial  Heaet-Blook. 

The  auricular  contractions  succeeding  synchronous  contractions  of  auricle  and 
ventricle  are  premature. 

the  more  nearly  do  the  commencements  of  auricular  and  ven- 
tricular systole  coincide.  To  a4,  occurring  immediately  after 
a  ventricular  contraction,  succeeds  an  a-a  period  of  0'70  second ; 
while  to  a  5,  which  occurs  in  the  middle  of  ventricular  con- 
traction, succeeds  a  period  of  0-55  second.     aQ  occurs  during 


COUPLED  RHYTHMS  179 

ventricular  diastole,  and  is  followed  by  an  auricular  contraction 
after  an  interval  of  0-70  second. 

The  block  in  this  case  was  suspected  on  auscultation.  A 
regular  rhythm  of  96  beats  per  minute  alternated  at  times 
with  a  much  less  frequent  and  irregular  rhythm,  long  pauses 
occurring  after  one,  two,  three,  or  more  beats.  During  the 
frequent  rate  the  first  sound  at  the  apex  was  followed  by  a 
short,  soft  whiff ;  with  the  infrequent  beats  the  murmur  was 
longer  and  louder,  replaced  a  considerable  portion  of  the  first 
sound,  and  ran  for  some  distance  into  the  short  pause.  As  the 
tracing  shows,  during  the  frequent  ventricular  rate  the  delay 
in  the  conduction  of  the  stimulus  from  auricle  to  ventricle  was 
so  great  that  ventricular  contraction  occurred  immediately 
before  the  succeeding  auricular  contraction,  and  at  a  time 
when  the  auricle  was  so  full  that  regurgitation  from  ventricle 
to  auricle  could  only  be  minimal,  however  great  the  incompe- 
tence of  the  valve.  With  infrequent  ventricular  beats,  how- 
ever, the  prolonged  rest  restored  conductivity  to  such  a  degree 
that  ventricular  contraction  occurred  relatively  early  in  relation 
to  the  succeeding  auricular  systole,  and  at  a  time  when,  the 
auricle  being  as  yet  not  nearly  full,  a  maximal  regurgitation 
was  possible,  and  a  longer  murmur  was,  in  consequence, 
audible. 

In  some  instances  the  synchronous  contraction  of  auricle  and 
ventricle  is  followed  by  a  ventricular  extra-systole.  This  is 
shown  in  Fig.  107,  which  was  obtained  from  a  case  of  full 
heart-block. 

An  undue  prolongation  of  diastole  may  also  be  followed  by  a 
premature  beat.  This  is  shown  in  Fig.  108,  obtained  from  a 
patient  whose  auricles  were  in  fibrillation.  Another  example 
is  shown  in  Fig.  109,  obtained  from  a  patient  whose  pulse 
often  beat  in  couples  for  hours  at  a  time.  The  sinus  rhythm 
was  extremely  mobile,  but  it  can  be  seen  that  the  first  ven- 
tricular extra-systole  succeeded  a  lengthened  diastole,  though 
at  the  end  of  the  tracing  an  even  longer  diastohc  period  was 
not  accompanied  by  an  extra-systole.  His  pulse  was  easily 
influenced  by  pressure  upon  the  left  vagus  nerve,  and  the 
diastohc  lengthening,  which  was  readily  produced  in  this  way, 
was  generally  followed  by  an  extra-systole,  which  might  recur 


ISO 


DISEASES  OF  THE  HEART 


for  a  few  beats  or  for  hours.  The  post-extra-systoHc  pause  in 
this  patient,  when  the  coupled  rhythm  was  continuous,  was 
also  generally  increased  by  pressure  upon  the  nerve. 

The  coupled  rhythm  shown  in  Fig.  110  differs  from  these 
cases  which  we  have  just  been  considering  in  that  both  heats 
are  in  response  to  similar  stimuli,  which,  however,  arise  in 
an  abnormal  situation  (nodal  rhythm).  It  is  this  type  of 
coupled  rhythm  that  Wenckebach  calls  "  true  "  bigeminy, 
inasmuch  as  beats  of  different  origin  cannot  be  considered 
as  "  true  "  twins. 


Brae/it'al 


Fig.  107.— Full  Heart-Block.     (W.  T.  R.) 

The  third  ventricular  contraction  coincides  with  an  auricular  contraction,  and  is 
quickly  followed  by  a  premature  ventricular  beat. 

Coupled  rhythm  is  apparently  invariably  associated  with 
evidence  of  cardiac  weakness,  and  very  often  with  mitral 
reflux.  Cases  in  which  coupled  rhythm  is  long  maintained 
are  usually  cases  of  chronic  heart  failure;  but  in  other  cases 
presenting  a  coupled  rhythm  for  shorter  periods,  the  degree  of 
cardiac  failure  may  be  equally  severe.  The  ventricular  rate  is 
usually  of  moderate  frequency. 

The  origin  of  a  coupled  rhythm  may  be  stated  as  follows : 
1.  The  ventricle  is   assumed  to  be  unduly  irritable,   and 
mitral   reflux   to    co-exist.     If    on   any    one   occasion,    from 


COUPLED  RHYTHMS 


181 


lengthening  of  diastole  or  synchronous  contraction  of  auricle 
and  ventrrcle,  the  ventricle  at  the  end  of  ventncular  con. 


'o 

to      . 

3  I 

go 

s  o 

>    r? 


to  tJ 


<S    o 


-fit 

H 


.action  is  imperfectly  e^ptiea  J^— Jf  ^  ^n.!^ 
auricle  wiU  rapidly  produce  so  great  a  cieg 


182 


DISEASES  OF  THE  HEART 


tkat  the  irritable  area  in  the  ventricular  wall  initiates  a 
premature  contraction. 

The  prematurity  of  the  contraction  insures  complete  empty- 
ing of  the  ventricle,  for  the  auricle  is  as  yet  relatively  empty, 
and  the  systoUc  reflux  is,  in  consequence,  full;  and  no  over- 
distension of  the  ventricle  will  occur  before  the  succeeding 
sinus  stimulus  arrives.  The  lengthened  diastole  which  thus 
ensues  entails  again  over-distension  of  the  ventricle,  even 
though  its  contractility  has  improved  during  the  longer  period 
of  rest,  and  so  an  imperfect  emptying  of  its  contents ;  and  the 
process  may  be  continued  indefijiitely. 

2.  In  cases  of  regularly  recurring  auricular  or  nodal  extra- 
systoles  the  process  is  comparable,  the  irritable  focus  being 


hi    I      05       [55    [       95       1-6     [^     1-0       I 


55        -95       -55 


■95 


as 


Fig.  110. — Nodal  Rhythih. 
Case  7,  p.  147.       True  bigeminy. 


situated  in  the  auricle.  If  the  auricle,  from  prolongation  of 
diastole  or  synchronous  contraction  of  auricle  and  ventricle, 
becomes  over-distended,  it  will  be  unable  to  empty  itself  com- 
pletely. With  the  succeeding  ventricular  systole  it  will  be 
rapidly  over- distended  by  the  reflux  of  blood  from  the  left 
ventricle,  and  the  excessive  intra-auricular  pressure  will  excite 
a  premature  contraction  in  auricle  or  node,  followed  in  due  time 
by  a  ventricular  systole.  As  this  ventricular  contraction  is  pre- 
mature, the  ventricle  is  incompletely  filled,  and  the  regurgitant 
blood  is  smaU  in  amount,  and  insufficient  to  distend  the  auricle 
to  such  a  degree  as  to  excite  a  new  contraction,  which  will 
only  obtain  when  the  next  sinus  stimulus  reaches  it.  The 
long  diastole,  however,  entails  again  auricular  over-distension, 
and  the  coupled  rhythm  will  continue  indefinitely  until  from 


COUPLED  RHYTHMS  183 

some  external  influence  (respiration,  exertion,  etc.)  the  flow  of 
blood  into  the  auricle  is  lessened,  and  with  an  auricular  con- 
traction of  sinus  origin  no  over-distension  of  its  cavity 
coincides . 

In  "  true  "  bigeminy  the  mechanism  is  similar,  the  only 
difference  being  that  beats  of  sinus  origin  are  replaced  by  beats 
which  arise  in  the  a.v.  node. 

There  is  probably  no  essential  difference  in  the  origin  of 
regularly  recurring  ventricular,  nodal,  or  auricular  extra- 
systoles.  The  difference  is  merely  a  difference  in  site  of  the 
irritable  area,  which  in  one  case  initiates  a  contraction  in  the 
ventricle,  in  the  second  in  the  node,  in  the  third  in  the  auricle. 

The  significance  of  coupled  rhythms  is  that  of  its  cause — 
extra-systole,  heart-block,  etc.  In  cases  where  it  is  produced 
by  the  administration  of  digitaHs,  it  is  an  indication  to  cease 
or  to  lessen  the  dose. 


CHAPTER  XV 
PAROXYSMAL  TACHYCARDIA 

The  Nodal  Form. 

The  occurrence  of  paroxysms  of  rapid  cardiac  action  was 
first  described  by  Cotton  in  1867,  and  since  then  numerous 
eases  have  been  reported,  and  many  theories  as  to  the  nature 
of  the  disturbance  have  been  suggested.  Considerable  light 
has  been  thrown  upon  the  subject  recently  by  means  of  the 
polygraph  and  the  electro-cardiograph,  and  it  appears  probable 
that  the  essential  feature  is  a  disturbance  of  the  intrinsic  cardiac 
mechanism,  which  is  not,  however,  always  of  the  same  nature, 
even  in  cases  which  otherwise  seem  comparable.  The  clinical 
symptoms  are  extremely  striking,  and  were  well  exemphfied  in 
the  following  case : 

An  iron-dresser,  aged  forty,  was  admitted  into  my  wards 
on  April  16,  1908,  complaining  of  attacks  of  breathlessness  and 
palpitation.  He  had  been  hable  to  these  for  seven  or  eight 
years,  'but  until  Christmas,  1907,  they  were  of  short  duration 
and  of  infrequent  occurrence,  and  rarely  ensued  save  upon 
exertion.  Since  then,  however,  they  had  been  more  frequent, 
and  occurred  when  he  was  at  rest  as  well  as  when  he  was 
at  work,  both  during  the  day  and  at  night,  and  had  even 
wakened  him  from  sleep.  At  first  they  only  lasted  for  at  most 
a  few  minutes,  but  recently  they  had  continued  for  several 
hours  at 'a  [time;  one  attack  persisted  for  two  days.  He  had 
found,  too,  that  he  was  more  easily  tired,  and_^  he^[had  felt 
weak  and  unfit  for  exertion,  though  he  had  continued  at  his 
work.  There  had  been  no  oedema,  giddiness,  headache,  or 
other  discomfort.  i 

He  had  always  been  a  healthy  man,  save  for  ]a  pleurisy  jten 
years  before.     His  work  was  arduous,  and  exposed  him  to 

184 


PAROXYSMAL  TACHYCARDIA  185 

extremes  of  temperature.  He  smoked  heavily,  and  frequently 
took  too  much  liquor. 

On  admission  he  was  found  to  be  a  well-built,  muscular  man. 
He  lay  quietly  in  bed  without  any  discomfort.  The  skin  per- 
spired fairly  freely.  There  was  no  oedema.  The  apex  impulse 
was  heaving  in  character  and  a  little  displaced  to  the  left,  and 
the  area  of  dulness  was  increased  in  the  same  direction.  The 
cardiac  sounds  were  pure ;  the  first  sound  at  the  apex  was  dull 
and  long,  and  the  second  aortic  sound  was  intoned.  The 
pulse  was  regular,  infrequent  (60  to  64),  full,  and  slow;  the 
arterial  walls  were  shghtly  thickened.  The  blood-pressure  was 
140-115  mm.  Hg.  The  urine  contained  a  haze  of  albumin. 
The  other  viscera  were  normal. 

For  the  first  few  days  after  admission  he  remained  in  bed 
and  experienced  no  discomfort,  and  felt  better  in  every  way; 
and  on  May  21  it  was  noted  that  the  apex  impulse  and  the  left 
border  of  cardiac  dulness  had  receded  to  their  normal  sites. 
The  urinary  output  was  free,  and  the  albumin  had  disappeared 
from  the  urine. 

On  the  evening  of  May  24,  however,  an  attack  of  palpitation 
ensued  at  7.45  p.m.  He  went  to  sleep  notwithstanding,  and 
when  he  awoke  at  2  a.m.  (May  25)  the  pulse-rate  was  normal. 
At  6  a.m.  the  tachycardia  recurred,  and  lasted  until  9.45  p.m. 
Both  attacks  commenced  and  ended  suddenly,  and  his  general 
condition  remained  unaltered.  He  sweated  fairly  freely,  but 
there  was  no  dyspnoea  or  discomfort  beyond  the  feeling  of 
palpitation,  and  he  took  the  ordinary  ward  diet  without  dis- 
turbance. The  liver  was  slightly  tender  during  the  afternoon 
of  the  25th. 

For  the  four  succeeding  days  he  remained  well,  but  on 
May  30  another  attack  supervened  at  9.40  a.m.,  and  continued 
until  3.45  a.m.  on  June  1,  when  it  ceased  as  suddenly  as  it  had 
commenced.  There  was  again  Uttle  subjective  discomfort 
beyond  the  palpitation,  but  he  complained  of  slight  headache. 
The  left  heart  dilated  a  httle  on  May  31,  and  the  Hver  became 
shghtly  tender  and  swollen ;  but  on  the  day  after  the  palpitation 
had  ceased  they  were  again  of  normal  size. 

The  cardiac  action  during  the  [attacks  was  always  quite 
regukir,  the  rate  varying  between  '134  and  180.     The  pulse 


186  DISEASES  OF  THE  HEART 

during  the  paroxysms  was  fairly  full,  but  very  quick  and 
soft,  the  systohc  blood-pressure  falling  to  85  mm.  during 
the  four  attacks  in  which  it  was  recorded,  as  contrasted 
with  125  to  115  mm.  in  the  intervals.  Sphygmographic 
tracings  at  the  higher  rates  were  often  monocrotic  and  the 
vessel  seemed  empty  between  the  beats.  The  pulsation  on 
the  front  of  the  chest  was  widespread  and  well-marked,  and 
the  cardiac  over-action  contrasted  strongly  with  the  softness 
of  the  pulse.  In  the  intervals  between  attacks  the  pulse 
numbered  56  to  68,  and  was  usually  quite  regular;  on  a  few 
occasions  an  extra-systole  (ventricular)  was  observed. 

He  remained  in  hospital  under  observation  until  August  21. 
On  dismissal  he  had  gained  a  stone  in  weight,  and  felt  in  good 
health  and  stronger  than  he  had  been,  but  he  had  never  made 
any  complaint  save  of  breathlessness  and  palpitation  during 
the  attacks. 

During  the  fourteen  weeks  twenty-one  attacks  of  tachycardia 
were  observed— May  24,  30;  June  4,  10  (three),  12,  13  (two), 
15,  18,  19  (two),  20  (two);  July  2,  5;  August  8,  13,  18  (two)— 
and  on  many  other  occasions  he  was  conscious  of  an  attack,  but 
of  such  short  duration  that  it  had  subsided  before  the  nurse's 
attention  was  attracted. 

The  attacks  commenced  suddenly  and  without  apparent 
cause,  and  occurred  at  any  period  of  the  twenty-four  hours, 
during  sleep  as  well  as  at  other  times.  Their  termination, 
which  was  as  abrupt  as  their  commencement,  was  observed  on 
several  occasions,  and  was  absolutely  sudden,  the  normal  rate 
instantly  succeeding  the  rapid  action.  He  was  but  slightly 
incommoded  during  the  attacks,  and  though  he  usually  appre- 
ciated their  commencement  and  end,  and  the  palpitation  during 
their  continuance,  he  was  not  always  conscious  of  the  tachy- 
cardia, and  was  accustomed  to  feel  his  pulse  to  ascertain  what 
the  rate  was.  He  had  no  dyspnoea,  orthopnoea,  cyanosis,  or 
oedema  during  the  attacks ;  his  skin,  however,  was  congested, 
and  he  sweated  fairly  freely,  but  he  took  his  food  and  went 
to  sleep  as  usual  during  a  paroxysm,  and  would  probably  have 
walked  about  save  that  he  was  confined  to  bed  by  order.  The 
attacks  varied  in  their  duration.  The  shortest  lasted  for  but 
a  few  minutes,  the  longest  for  forty-two  hours. 


PAROXYSMAL  TACHYCARDIA  187 

He  was  again  admitted  to  hospital  on  June  11,  1910.  He 
had  maintained  fair  health  in  the  interval,  and  had  continued 
his  work  as  an  iron-dresser,  though  attacks  of  palpitation  of 
short  duration  recurred  about  every  fortnight.  In  March, 
1910,  however,  an  attack  lasted  for  two  days,  and  he  was  off 
work  for  a  week.  On  June  7  an  attack  commenced  and  con- 
tinued without  interruption  until  June  11,  the  longest  attack 
that  he  had  had.  This  paroxysm  was  preceded  by  abdominal 
pain,  and  was  accompanied  by  nausea  and  retching,  and  sub- 
sided after  a  bout  of  vomiting,  after  which  the  pain  disappeared. 
He  remained  in  hospital  until  July  5,  and  had  only  a  few 
paroxysms,  the  longest  of  which  lasted  for  twelve  hours.  The 
highest  pulse-rate  recorded  was  180.  His  general  condition 
was  good,  and  no  change  was  found  in  the  viscera. 


a,  V     a  V 


't^-^'^,^.2^.v!!c^>^^^v!::"''''V'-vr>j 


Fig.  111. — Paroxysmal  Tachycardia. 
The  a-c  interval  is  less  than  O'lO  second;  P.R.,  180. 

Tracings  (Fig.  Ill)  were  obtained  on  many  occasions  during 
the  paroxysms,  and  always  presented  the  same  features,  a 
small  c  wave  followed  by  a  large  and  early  v,  indicative  of 
venous  engorgement,  and  succeeded,  ere  the  base-line  was 
reached,  by  a  distinct  a,  which  was  almost  synchronous  with  the 
a  wave  in  the  apex  curve.  The  transmission  time  is  short,  for  c 
in  the  cervical  curve  rapidly  succeeds  the  rise  of  the  ventricular 
impulse.     The  a-c  interval  is  regularly  less  than  0-10  second. 

There  is  a  marked  similarity  between  attacks  even  in  different 
patients.  The  onset  of  the  tachycardia  is  sudden  and  appar- 
ently instantaneous,  and  the  termination  is  equally  abrupt. 
Attacks  may  commence  without  obvious  cause,  but  are  fre- 
quently, especially  in  the  earlier  phases,  the  sequel  to  physical 
exertion.  As  time  goes  on,  the  degree  of  exertion  required 
often  diminishes,  so  that  attacks  ensue  on  apparently  trivial 


188  DISEASES  OF  THE  HEART 

physical  strain.  Sometimes  they  follow  straining  at  stool. 
In  a  patient  under  my  care  they  at  first  succeeded  severe  fits 
of  coughing,  during  which  the  patient  became  extremely  livid, 
her  face  swelling  rapidly  to  nearly  double  its  usual  size,  and 
the  jugular  veins  becoming  distended  to  three  or  four  times 
their  usual  diameter.  The  pulse  became  extremely  frequent 
and  uncountable,  and  lost  markedly  in  volume  and  strength, 
and  continued  in  this  way  for  several  minutes,  when  the 
infrequent  rate  was  rapidty  resumed. 

jSometimes  they  seem  to  succeed  mental  excitement,  and,  in 
consequence,  they  not  infrequently  occur  'in  the  consulting- 
room,  or  at  demonstration  in  the  wards .  In  one  of  my  patients, 
who  required  operation  on  account  of  acute  appendicitis,  the 
frequency  of  the  pulse-rate  excited  apprehension  of  widespread 
peritoneal  involvement,  which  proved,  however,  to  be  un- 
founded, and  the  pulse  rapidly  resumed  its  normal  rate  after 
operation.  Flatulent  distension  of  the  stomach,  too,  may  be 
an  exciting  cause. 

The  cardiac  phenomena  are  characteristic.  The  pulse-rate 
is  greatly  increased,  and  numbers  150  and  upwards;  160  to 
180  seem  to  be  common  figures,  but  I  have  records  of  214  and 
234  beats  per  minute,  and  even  higher  figures  have  been  re- 
ported, the  maximum  being  about  300.  Coincidently  the  pulse 
loses  both  in  force  and  in  volume,  and  becomes  small  and  soft 
and  quick,  irrespective  of  its  previous  character.  The  cardiac 
pulsations,  too.  become  exaggerated,  pulsation]  being  notice- 
able in  several  interspaces  on  both  sides  of  the  sternum,  though 
diffuse  and  badly  sustained.  The  whole  chest  may  shake,  and 
the  vehemence  of  the  heart's  contractions  contrasts  in  a  striking 
way  with  the  smallness  and  softness  of  the  pulse. 

The  symptoms  of  the  patient  seem  to  depend  upon  the 
amount  of  the  cardiac  reserve.  In  uncomplicated  cases  the^^ 
are  often  surprisingly  slight,  and  the  consciousness  of  the  heart- 
beats may  be  the  sole  subjective  sensation.  In  long-continued 
paroxysms,  however,  evidence  of  venous  stasis  [may  be 
observed — breathlessness,  congestion  of  the  liver,  albuminuria, 
a  scanty  concentrated  urine,  and  oedema  of  the  extremities. 
In  patients  who  are  already  seriously  ill  the  occurrence  of 
tachycardia  rapidly  augments  the  distress. 


PAROXYSMAL  TACHYCARDIA  189 

A  labourer,  aged  thirty-eight,  was  admitted  into  my  wards 
complaining  of  headache,  palpitation,  and  general  weakness 
of  six  months'  duration.  The  earliest  symptom  was  the 
occurrence  of  attacks  of  palpitation,  which  were  generally 
nocturnal,  and  rarely  came  on  during  the  day.  At  first  they 
occurred  about  once  a  week,  and  lasted  from  thirty  minutes 
to  three  hours,  but  they  had  gradually  become  more  frequent 
and  of  longer  duration.  He  noticed  that  he  was  easily  made 
short  of  breath  upon  exertion,  and  his  weakness  increased  so 
that  he  was  forced  to  take  to  bed  a  fortnight  before  admission 
into  hospital.  Since  then  the  palpitation  had  not  recurred, 
but  he  had  had  several  attacks  of  breathlessness . 

On  admission  he  M^as  extremely  ill,  in  full  orthopnoea,  the 
respirations  being  laboured  and  cychc.  The  heart  was  greatly 
enlarged,  and  double  aortic  murmurs  were  audible  on  auscul- 
tation. The  hver  was  enlarged,  and  the  urine  contained  much 
albumin.  The  pulse  was  regular  and  shotty,  and  numbered  88, 
In  ten  days  improvement  was  marked,  and  he  was  breathing 
easily  and  lying  low  in  bed.  The  liver  was  smaller,  and  the 
albuminuria  was  trifling.  Four  days  later,  however,  an  attack 
of  tachycardia  ensued,  and  lasted  from  9  a.m.  until  5  p.m.,  the 
pulse-rate  varying  between  152  and  180;  and  all  the  old 
symptoms  at  once  recurred.  Next  day  he  was  much  better, 
but  the  breathing  was  still  difficult  and  cyclic,  and  he  required 
three  pillows.  The  symptoms  continued,  and  a  few  days 
later  he  had  an  attack  of  vomiting,  during  which  he  nearly 
died,  his  face  becoming  livid,  and  the  jugular  veins  greatly 
distended.  Five  days  later  Janother  attack  of  tachycardia 
supervened,  and  though  it  only  lasted  for  an  hour,  notably 
intensified  his  distress.  The  pulse-rate,  too,  only  fell  to  110 
after  the  attack  had  passed  off.  In  the  evening  another 
paroxysm  ensued,  the  pulse  numbering  about  200.  The 
cyanosis  became  extreme  and  the  dyspnoea  urgent,  and  after 
three  hours  the  heart  suddenly  ceased  to  beat. 

On  examination  the  heart  was  very  large,  weighing 
25|  ounces.  The  aortic  valve  was  notably  incompetent  from 
chronic  sclerotic  changes,  the  aorta  was  very  atheromatous, 
and  the  orifices  of  the  coronary  arteries  were  considerably 
narrowed.     The  kidneys  showed  widespread  fibroid  change. 


190  DISEASES  OF  THE  HEART 

In  this  case  the  tachycardia  seemed  directly  responsible  for 
the  fatal  termination,  as  improvement  had  been  considerable 
after  his  admission  to  hospital.  The  post-mortem  examination, 
however,  showed  widespread  valvular  and  myocardial  disease, 
so  that  the  cardiac  reserve  must  have  been  small. 

A  similar  sequence  was  observed  in  a  case  of  chronic  bron- 
chitis and  emphysema.  The  paroxysms  were  sharply  related 
to  bouts  of  coughing,  and  at  first  ceased  shortly  after  the 
cough,  but  later  on  continued  indefinitel3^  and  rapidly  pro- 
duced fatal  cardiac  failure. 

A  married  woman,  aged  fifty-three,  was  admitted  to  hospital, 
complaining  of  a  cough  and  spit  and  severe  sickness.  She  had 
had  an  attack  of  pleurisy  twenty  years  before,  and  had  been 
subject  to  a  winter  cough  ever  since.  A  fortnight  before  her 
admission  she  caught  cold,  and  the  cough  became  more  trouble- 
some. Three  days  later  vomiting  ensued  and  continued.  It 
was,  in  part  at  any  rate,  induced  by  the  cough,  and  prevented 
her  from  retaining  any  food  at  all,  and  she  had  become  very 
exhausted. 

She  was  a  big,  stout  woman,  but  flabby  and  soft,  and  on 
admission  was  verj^  ill,  the  mucous  membranes  being  extremely 
livid,  and  the  feet  oedematous.  The  finger-tips  were  slightly 
clubbed.  She  retched  continuously,  but  only  brought  up  a 
Httle  mucus.  The  pulse  was  small,  and  so  frequent  as  to  be 
uncountable.  The  heart  was  greatly  enlarged,  and  a  systolic 
murmur  was  audible  at  the  apex.  There  was  widespread 
bronchitis,  and  a  chronic  consohdation  at  the  right  apex. 
The  urine  contained  albumin  in  abundance. 

For  a  few  days  after  admission  she  improved  considerably, 
the  vomiting  ceasing,  and  enabhng  her  to  retain  a  fair  quantity 
of  fluid  food;  but  she  had  at  times  severe  bouts  of  cough, 
during  which  she  became  extremely  hvid,  the  face  swelhng 
enormously,  and  the  jugular  veins  becoming  distended  to  many 
times  their  usual  size.  The  pulse  became  tiny  and  very 
frequent  and  uncountable,  and  she  appeared  at  the  point  of 
death.  The  symptoms,  however,  rapidly  subsided  when  the 
coughing  ceased.  On  October  20,  after  a  restless  night,  she 
had  a  severe  fit  of  coughing,  and  was  collapsed  and  weak  for 
some  hours.     At  11  a.m.  on  the  21st  the  pulse  was  found  to 


PAROXYSMAL  TACHYCARDIA  191 

be  extremely  rapid  (200),  and  small  and  soft,  but  she  did  not 
seem  to  be  notably  distressed.  In  the  evening  the  vomiting 
recurred,  and  she  was  extremely  weak  and  feeble,  but  next 
morning  she  had  improved,  and  the  pulse  w^as  fuller  and 
stronger,  and  numbered  80.  A  few  extra-systoles  were  observed 
at  this  time.  The  tachycardia,  however,  returned  at  noon  on 
October  23,  and  continued  until  her  death  on  the  25th  from 
cardiac  failure. 

Ko  cervical  tracings  were  obtained  in  this  patient,  but  epi- 
gastric curves  showed  a  rate  of  222  beats  per  minute  on 
October  21,  and  234  per  minute  on  October  23. 

All  the  available  evidence  goes  to  show  that  paroxysms  of 
tachycardia  are  due  to  the  inception  of  a  new  cardiac  rhytlim, 
the  contractions  originating  in  some  abnormal  situation  in  the 
heart.  The  pulse-rate,  it  is  true,  varies  considerably  in  indi- 
viduals, and  rates  approximating  to  the  lower  figures  reached 
in  paroxysmal  tachycardia  have  been  recorded  in  patients 
whose  cervical  curves  were  of  normal  type ;  but  the  onset  and 
the  cessation  of  the  frequent  action  are  almost  invariably 
gradual,  and  a  sudden  change  is  rarely  seen.  In  only  one  case 
have  I  observed  a  comparable  change  in  rate. 

The  patient,  a  labourer  aged  fiity-four,  was  admitted  to 
hospital  complaining  of  breathlessness  and  praecordial  pain  of 
three  weeks'  duration.  He  had  suffered  from  acute  rheu- 
matism five  years  previously,  and  had  since  then  been  subject 
to  breathlessness  and  palpitation  upon  exertion,  but  these 
had  not  interfered  with  his  work.  Three  weeks  before 
admission,  however,  after  a  severe  strain  at  his  work,  he 
suddenly  became  extremely  short  of  breath,  and  felt  his  heart 
fluttering,  and  experienced  severe  pain  in  the  prsecordial 
region.  These  symptoms  steadily  progressed;  his  feet  and 
legs  began  to  swell,  and  he  was  forced  to  seek  admission  to 
hospital. 

He  was  a  well-built  man  and  weU  nourished.  On  admission 
he  was  extremely  breathless,  and  had  to  sit  upright  in  his  bed. 
The  cedema  extended  as  high  as  the  sacrum,  but  was  not 
excessive.  His  heart  was  large,  and  double  aortic  murmurs 
were  audible  over  the  sternum.  The  pulse  was  very  shotty 
but  quite  regular,  and  numbered  92.     His  progress  was  con- 


192  DISEASES  OF  THE  HEART 

tinuousl}'  in  the  right  direction,  and  he  made  a  good  conva- 
lescence. 

The  point  of  interest  lay  in  pulse  disturbances  which  appeared 
four  clays  after  admission  at  a  time  when  improvement  was 
already  manifest.  The  oedema  had  gone,  and  he  was  lying 
low  in  bed,  and  feeling  quite  comfortable.  The  breathing  was 
less  difficult,  but  was  now  for  the  first  time  Cheyne-Stokes  in 
character,  the  periods  of  apnoea  being  of  considerable  length. 
The  pulse  was  infrequent  and  irregular,  little  runs  of  two,  three, 
or  more  beats  at  a  quicker  rate  occurring  at  frequent  intervals 
and  irrespective  of  the  respirator}^  phases.  The  tracings  were 
always  of  the  same  character  whatever  the  duration  of  the 
"tachycardia."  In  Fig.  112  the  first  three  pulse  periods  are 
practically  equal ;  period  4  is  shorter,  period  5  is  shorter  still, 
period  6  is  longer,  but  not  so  long  as  the  first  three,  and  the 
initial  rhythm  then  recurs.  In  Fig.  113  the  first  two  periods 
are  long  and  equal,  3  is  shorter,  and  then  comes  a  series  of  25 
beats  in  rapid  succession  before  the  slower  rhythm  is  resumed. 
The  pulse  periods  of  the  frequent  rate  are  practically  equal, 
save  in  the  case  of  beats  8  and  9,  period  8  being  shorter  and 
period  9  longer  than  the  others.  The  jugular  curve  shows 
that  all  the  beats  are  apparently  of  sinus  rhythm,  the  a-c 
interval  being  of  normal  duration,  save  in  the  case  of  beat  9, 
where  it  is  short.  The  ventricular  contraction  is  premature, 
but  the  auricular  rhythm  is  unaltered,  so  that  beat  9  is  a 
ventricular  extra-systole. 

The  case  is,  of  course,  not  one  of  paroxj^smal  "  tachycardia," 
though  it  shows  an  abrupt  change  from  a  pulse-rate  of  about 
63  beats  per  minute  to  one  of  117,  the  normal  sinus  rhythm 
continuing  unchanged.  There  was  no  constant  relationship 
between  the  cardiac  and  the  respiratory  irregularities,  and 
both  the  pulse  and  the  respirations  became  regular  mthin 
three  or  four  days. 

The  cervical  curves  in  paroxj^smal  tachycardia  are  often 
difficult  to  interpret  on  account  of  the  frequency  of  the  cardiac 
contractions,  for  with  a  pulse-rate  of  180  or  more  diastole  is 
so  short  that  auricular  systole  occurs  before  the  preceding 
ventricular  contraction  has  ceased,  and  v  and  a  are  inex- 
tricably mingled.     In  some  cases,   however,   they  are  more 


WA/U^'WU'AJ'^ 


Fig.  113.— a  Paroxysm  of  Fi 
Beat! 


The  rhythm  of  the  he 


^^      vac    vq  c    V  d  c    u  AC  V  a  c    «  ^'^yf 


Fig. 
res  showing  the  sudden  transition  fro 


[To  face  page  192. 


JvJV^JMUJiAAJiJiWJi 

Fig.  112. 
The  rhythm  of  fcho  heart  varies,  bub  the  o-c  interval  is  always  normal. 


JiAji/i_i.iJUyijjijij/j4WJiAjA/uUwU'iU'j^/j-AJ^iiu^i/ii'/u%i        |i,J.jJV^/«JiJjiMJj'JJ'^ 


Fig.  113.— a  P 


oir  Frequent  Caediac  Beats  with  a  Normal  a-c  Interval. 
Beat  9  is  a  ventricular  estra-syatole. 


Fio.  114. — Paroxysmal  Tachycardia. 
Curves  showing  the  sudden  transition  from  boats  with  a  short  a-c  interval  to  those  with  a  normal  a-c  interval. 


PAROXYSMAL  TACHYCARDIA  193 

intelligible,  and  v  and  a  are  distinct,  perhaps  as  the  result  of 
insufficiency  of  the  tricuspid  valve,  so  that  v  occurs  early  in 
the  cycle  and  precedes  a. 

Fig.  Ill  was  obtained  when  the  pulse  numbered  180  per 
minute.  The  cervical  curve  is  regular  and  shows  three  waves, 
the  smallest  being  c.  This  is  rapidly  succeeded  by  an  early 
and  prominent  v,  on  the  downstroke  of  which  a  is  distinct,  and 
precedes  c  by  less  than  0-10  second.  The  apical  curve  is  also 
clear,  and  a  is  rapidly  succeeded  by  v  before  the  base-line  has 
been  reached.  In  Fig.  114  the  transition  between  the  normal 
and  abnormal  rhythm  is  distinctly  shown.  The  pulse-rate  is 
gradually  slowing  before  the  central  ordinates  (one  beat),  but 
the  essential  change  occurs  between  the  second  and  third  beats 
following    them.     In   the   cervical   curve   a   is    unfortunately 


Fig.  115. — Paroxysmal  Tachycaedia. 
The  a-c  interval  is  less  than  O'lO  second;  P.R.,  214. 

mingled  with  v  and  somewhat  indefinite,  but  the  apical  curve 
is  clear.  The  a-c  interval  in  the  former  changes  suddenly 
from  less  than  0-10  to  0*20  second;  and  the  A.V.  interval  in  the 
latter  from  0-05  second  to  nearly  0-10  second.  As  has  been 
already  shown  (p.  127),  so  short  an  a-c  interval  indicates  that 
the  contractions  originate  between  the  auricle  and  the  ventricle, 
and  are  not  in  response  to  normal  stimuh. 

The  majority  of  the  curves  which  have  been  published  are 
similar  to  those  which  have  just  been  described,  and  another 
example  is  shown  in  Fig,  115  with  a  pulse-rate  of  214.  Lewis, 
too,  has  published  comparable  electro-cardiograms  (Fig.  218, 
Plate  II.),  with  a  short  P.R,  interval  and  an  inverted  P,  so 
that  the  evidence  seems  complete  that  attacks  of  tachycardia 
may  be  due  to  the  inception  of  a  nodal  rhythm  as  the  curves 
are  similar,  save  in  the  frequency  of  the  contractions,  to  those 
which  I  have  already  designated  by  this  term, 

13 


194  DISEASES  OF  THE  HEART 

Experimental  evidence  (Lewis,  Hirschfelder),  however, 
strongly  suggests  that  similar  paroxysms  may  occur  from 
stimuli  arising  lower  down  in  the  ventricle  which  precedes  the 
auricle  in  its  contraction.  A  "  retrograde  "  contraction  of  the 
auricle  rarely  succeeds  an  isolated  ventricular  premature 
systole,  but  if  the  latter  recurs  for  several  beats,  the  auricular 
contractions  change  their  rhythm,  apparently  in  response  to 
stimuli  passing  backwards  from  the  ventricle. 

Variations  in  the  exact  site  of  origin  of  the  stimuli  may 
conceivably  produce  slight  variations  in  polygraphic  and 
electric  curves.  If  they  arise  in  the  node,  the  auricular  con- 
tractions precede  the  ventricular;  but  if  lower  down,  the- 
auricular  and  ventricular  responses  may  be  simultaneous,*  and 
if  lower  still,  the  ventricles  may  contract  first.  In  each  case^ 
however,  the  a-c  or  the  c-a  interval  is  excessively  short. 

It  seems  probable,  too,  that  paroxysmal  tachycardia  may 
be  due  to  auricular  flutter,  and  that  many  of  the  cases  hithertO' 
pubhshed  as  examples  of  the  former  are  really  cases  of  the 
latter.  The  patient  from  whom  Fig.  115  was  obtained,  for 
example,  had  certainly  auricular  flutter  a  few  days  after  the 
tracing  was  obtained,  and  varying  degrees  of  conductivity 
might  conceivably  account  for  the  varying  number  of  the 
ventricular  contractions.  Sudden  doubUng  or  halving  of  the 
ventricular  rate — at  one  time  supposed  to  be  characteristic  of 
paroxysmal  tachycardia — is  probably  always  indicative  of 
auricular  flutter.  Hertz  and  Goodhart's  case  probably  comes 
under  this  category. 

The  essential  feature  of  paroxysmal  tachycardia  appears  tO' 
be  the  inception  of  a  new  site  of  stimulus  production.  The 
cause  of  this  is  obscure,  but  is  probably  to  be  sought  for  apart 
from  organic  lesions  of  the  a.v.  tissues,  for  in  those  cases  which 
I  have  described  as  "nodal  rhj'thm,"  where  definite  lesions 
were  found  post-mortem,  the  pulse-rate  was  never  extremely 
frequent,  and  no  sudden  changes  in  rate  ever  ensued.  The 
causes  which  produce  premature  systoles  are  probably  those 

*  A  case  recorded  by  Falconer  and  Dean  ("  Heart,"  1912-13,  vol.  iv.,  p.  137) 
showed  short  paroxysms  of  tachycardia  during  which  the  a  and  c  waves  in  the 
cervical  curve  were  synchronous ;  and  on  post-mortem  examination  an  acute? 
inflammatory  lesion  in  the  middle  third  of  the  a.v.  bundle. 


PAROXYSMAL  TACHYCARDIA  195 

wliicli  may  produce  paroxysms  of  frequent  contractions,  but  the 
nature  of  the  underlying  excitability  of  the  parts  concerned 
still  awaits  elucidation.  A.  M.  Kennedy  has  examined  the  a.v, 
tissues  in  one  case,  and  found  that  they  were  apparently 
normal,  though  the  s.a.  node  was  involved  in  a  chronic  and  an 
acute  injBlammatory  reaction. 

The  coincidence  of  the  auricular  and  the  ventricular  con- 
tractions explains  several  of  the  characteristic  features  of  the 
paroxysms.  During  ventricular  systole  the  auriculo-ventric- 
ular  valves  are  shut,  and  the  auricle  contracting  simultaneously 
is,  in  consequence,  unable  to  supply  the  ventricle  with  its 
normal  quantity  of  blood.  The  ventricular  output  is  thus  les- 
sened, and  the  pulse  loses  both  in  volume  and  in  force. 

The  auricular  contraction  drives  the  blood  backward  into 
the  veins,  and  thus  initiates  venous  stasis ;  which,  if  the 
paroxysm  is  prolonged,  rapidly  becomes  serious  in  its  degree, 
the  lungs  and  the  liver  becoming  engorged,  and  oedema  making 
its  appearance  in  the  dependent  parts.  The  pulsations  in  the 
neck,  too,  become  larger  and  more  distinct. 

The  obstacle  to  the  output  from  the  auricle  stimulates  it 
to  increased  effort,  and  the  pulsations  on  the  front  of  the  chest 
become  more  forcible  and  more  widespread,  and  the  apparent 
strength  of  the  cardiac  contractions  contrasts  markedly  with 
the  smallness  and  softness  of  the  arterial  pulse. 

At  the  present  time  accurate  data  of  the  incidence  of 
paroxysmal  tachycardia  are  necessarily  awanting,  for  the 
nodal  rhj'thms,  auricular  fibrillation,  and  auricular  flutter  have 
only  recently  been  differentiated  from  each  other,  and  our 
present  knowledge  of  the  relationship  between  them  is  ex- 
tremely scanty.  Electrical  stimulation  of  the  auricle  may 
produce  extra-systoles,  and,  if  continued,  auricular  flutter,  and 
in  time  auricular  fibrillation ;  and  James  Mackenzie  has  observed 
flutter  pass  into  fibrillation  in  patients  under  the  influence  of 
digitalis.  (I  have  once  seen  this  occur.)  Some  of  the  cases  of 
paroxysmal  tachj^cardia  show  at  one  time  tracings  of  "nodal 
rhythm,"  and  later  on  of  flutter;  and  in  the  constant  nodal 
rhythms  extra-systoles  have  been  observed  to  precede  the 
onset  of  the  rhythm.  It  seems  probable  that  extra-systoles, 
the  nodal  rhythms  and  auricular  flutter,  are  closely  allied  and 


196  DISEASES  OF  THE  HEART 

that  the  last  two  are  merely  series  of  extra-systoles  originating 
in  different  situations.  Lewis  thinks  that  auricular  fibrillation 
is  of  similar  nature,  the  stimuli  arising  in  many  places  in  the 
auricular  muscle  instead  of  in  one  constant  situation;  but 
Gaskell's  theory  that  fibrillation  is  due  to  defects  in  conduction 
between  the  auricular  muscle  cells  seems  a  more  probable 
explanation. 

It  is,  however,  apparent  that  paroxysmal  tachycardia, 
auricular  flutter,  and  auricular  fibrillation  may  occur  in  both 
sexes  and  at  every  age,  though  they  are  all  less  frequent  in 
early  childhood ;  in  every  form  of  organic  cardiac  disease,  and 
in  hearts  that  are  apparently  normal;  in  hypertrophied  hearts, 
and  in  hearts  of  normal  size.  They  may  arise  suddenly  and 
cease  suddenly,  both  in  experiment  and  in  the  clinique,  and 
may  thus  be  the  result  of  functional  disturbances.  Fibrillation 
and  nodal  rhythm  may  also  be  permanent,  and  are  then,  in  all 
probability,  the  sequel  to  organic  disease. 

The  prognosis  in  paroxysmal  tachycardia  must  be  based 
upon  several  factors.     Paroxysms  of  short  duration  and  infre- 
quent occurrence,  which  have  never  produced  any  signs  of 
cardiac  insufficiency,  occurring  in  patients  with  no  obvious 
diminution  in  the   field  of   response,   are   of   little  practical 
importance,  save  that  they  indicate  a  tendency  to  functional 
disturbance  which  may  in  time  prove  serious.     Herringham* 
states  that  the  condition  seems  always  to  tend  to  get  worse 
and  in  the  end  to  kill,  and  that  after  thirty  the  patient  is  never 
safe,  though  the  progress  may  be  slow,  since  people  who  have 
been  affected  in  childhood  have  been  known  to  pass  fifty  years. 
On  the  other  hand,  paroxysms  of  considerable  duration  and 
frequent  occurrence,  which  produce  signs  of  obvious  cardiac 
distress  and  obtain  in  patients  whose  hearts  in  the  intervals 
exhibit  little  cardiac  reserve,  are  in  a  condition  of  extreme 
danger.     A  paroxysm  which  la  its  for  two  or  three  days  seems 
always    to    produce    symptoms,    and    the    duration    of    the 
paroxysms  is  probably  of  most  importance  in  this  respect. 

The  treatment  of  the  paroxysms  is  still  unsatisfactory.  The 
vast  majority  of  attacks  end  spontaneously,  and  the  patient  is 
restored  to  his  usual  health,  but  there  is  little  that  can  be  done 

*  Edin.  Med.  Journ.,  1897,  N.S.,  vol.  i.,  p.  '^m. 


PAROXYSMAL  TACHYCARDIA  197 

to  induce  the  cessation  of  the  frequent  action.  I  have  seen 
attacks  cease  after  deep  breathing,  holding  the  breath,  exertion, 
the  act  of  vomiting,  the  appHcation  of  fomentations  to  the 
praecordia,  and  they  have  been  described  as  terminating  after 
pressure  had  been  exercised  upon  the  chest  or  upon  the  vagus 
nerve  in  the  neck.  But  everyone  is  agreed  that  those  measures 
usually  fail,  and  that  their  effects  are  rarely  uniform  even  in 
the  same  patient.  Digitalis,  too,  has  proved  equally  useless 
in  my  hands,  although  good  results  have  been  recorded  after 
its  administration. 

Much,  however,  can  be  done  in  the  intervals  to  lessen  the 
frequency  of  the  attacks.  A  careful  detailed  survey  of  the 
case  usually  shows  some  manifest  error  in  the  mode  of  life,  or 
some  functional  disturbance  in  one  or  other  of  the  viscera. 
As  Herringham  points  out,  the  over-use  of  tea,  coffee,  alcohol, 
or  tobacco,  or  some  digestive  disturbance,  are  sometimes 
responsible.  The  cardiac  reserve  m.a.ry  be  limited,  even  in  the 
absence  of  organic  valvular  or  myocardial  disease,  and  the 
usual  modes  of  treatment  are  necessarily  indicated.  Or  the 
cares  of  business  or  domestic  worries  may  press  unduly  upon 
the  patient. 

It  may  appear  unnecessary  to  limit  the  phj^sical  exercise  of 
these  patients  if,  when  seen  between  attacks,  their  general 
health  and  nutrition  seem  unimpaired,  but  my  personal  ex- 
perience has  taught  me  caution  in  this  respect.  A  paroxysm 
in  esse  is  always  a  period  of  danger,  for  it  is  impossible  tc 
predict  its  duration,  and  if  it  continues  for  more  than  a  day 
or  two,  definite  signs  of  cardiac  failure  are  sure  to  appear. 
The  heart,  too,  is  unduly  irritable,  whatever  the  source  of  this 
may  be,  and  an  irritable  organ  is  hypersensitive  to  strain  and 
stress,  so  that  it  is  generally  advisable  to  exercise  precautions 
in  this  direction ;  and  if  the  attacks  are  frequent,  however  short 
their  duration,  or  if  any  evidence  of  cardiac  insufficiency  is 
present,  the  patient  should  be  confined  for  a  time  to  bed.  In 
the  milder  cases  less  restriction  is  indicated.  The  obvious 
errors  should  at  the  same  time  be  corrected,  special  attention 
being  paid  to  the  alimentary  tract,  and  a  general  tonic  may  be 
added.     Small  doses  of  digitalis  seem  in  many  cases  to  help. 


CHAPTER  XVI 

AURICULAR  FLUTTER 

In  1905  the  late  G.  A.  Gibson  and  W.  T.  Ritchie  reported  a 
case  in  which  polygraphic  tracings  showed  that  the  auricular 
contractions  were  extremely  frequent  (about  270  per  minute) 
and  perfectly  rhj^thmic,  though  the  ventricular  contractions  were 
infrequent  (about  35  per  minute)  and  fairly  regular,  the  result, 
apparently,  of  full  heart-block;  and  in  1906  they  recorded  a 
second  case  in  which  the  auricular  contractions  numbered 
about  350,  while  the  ventricular  contractions  numbered  about 
40.  In  1909  Morrison  reported  a  case  of  very  rapid  auricular 
contractions,  in  which  the  ventricles  usually  beat  at  haK  the 
auricular  rate;  and  in  the  same  year  Hertz  and  Goodhart 
described  a  fourth  case  in  which  the  ventricles  contracted 
about  80  times  per  minute,  while  the  auricles  beat  four  times 
as  frequently.  In  1910  Jolly  and  Ritchie*  published  the 
results  of  electro-cardiographic  investigations  of  the  case 
which  had  been  reported  in  1905,  and  showed  that  there  were 
distinct  differences  between  the  curves  of  the  auricular  con- 
tractions in  this  case  and  in  patients  in  whom  the  auricles  were 
in  fibrillation.  The  rate  was  less  frequent,  the  rhythm  was 
quite  regular,  and  tracings  showed  with  Derivations  II.  and 
III.  a  diphasic  deflexion.  MacWilliam  had  already  found  that 
the  application  of  a  faradic  current  to  the  auricles  might — in 
experiment — produce  a  rapid  co-ordinate  "  flutter  "  of  the 
auricles,  the  contractions  originating  in  the  stimulated  area; 
and  Jolly  and  Ritchie,  recognizing  the  similarity  of  the  clinical 
and  experimental  tracings,  designated  the  condition  "auric- 
ular flutter."     Recent  papers   by  Ritchief  and  Lewis, J  with 

*  Heart,  1910-11,  vol.  ii.,  p.  177. 
t  Edin.  Med.  Journ.,  1912,  N.S.,  vol.  ix.,  p.  485. 
%  Heart,  1912-13,  vol.  iv.,  p.  171. 
198 


AURICULAR  FLUTTER  199 

tracings  from  other  cases,  seem  to  have  estabhshed  the 
identit}^  of  a  new  rhythm,  and  one,  too,  that  is  of  frequent 
occurrence. 

Auricular  flutter  is  most  readily  recognized  in  electro- 
cardiograms, and  is  well  shown  in  Fig.  116,  which  is 
reproduced  by  kind  permission  of  W.  T.  Ritchie.  The  ven- 
tricular contractions  show  well-marked  R  and  8  deflexions, 
and  the  successive  beats  are  separated  from  each  other  by 
regularly  recurring  diphasic  waves  of  considerable  size,  which 
in  this  figure  overlap  and  obliterate  the  Q  and  T  deflections  of 
the  normal  ventricular  complex.  The  auricular  waves  are 
regular  in  rhythm,  and  number  281  per  minute,  and  differ  in 
their  regularity,  their  less  frequent  rate,  and  their  diphasic 
character  from  the  waves  which  are  present  in  auricular 
fibrillation.  The  ventricular  rate  is  almost  constant  (72-25  per 
minute). 

R 


'  '  '  '  ff 

iiiiiiiiiiiiiiiiiiiiituuuuiiiiiiiuiiiiuiiiUJiiiimuiiikiiiiiiiiiiiUiiuuiniiiiiiiAiiiiiiiniimiiimuiiiuuiiiiHUiiiiiiii 

Fig.  116. — ELECTEO-CARMOGEAjii  OF  Atjeicular  Flitttee.     (W.  T.  R.) 

The  rate  of  the  ventricular  contractions  varies  considerably 
in  auricular  flutter,  and  if  it  is  infrequent  the  auricular  waves 
may  be  readily  seen  in  polygraphic  tracings  (Figs.  117,  118). 
Their  size  varies.  The  waves  synchronous  with  the  carotid 
impulse  and  those  immediatelj^  succeeding  it  are  ample,  as 
auricular  contraction  coincides  with  ventricular  contraction 
(c  and  v),  and  the  auricle  is  thus  unable  to  force  its  contents 
through  the  closed  auriculo-ventricular  valve  ;  the  blood 
is,  in  consequence,  thrown  back  into  the  jugular  vein.  As 
ventricular  diastole  ensues,  the  waves  at  first  are  smaller, 
but  they  again  increase  in  size  as  systole  approaches,  owing  to 
the  increasing  fulness  of  the  ventricle  and  the  increasing  diffi- 
culty in  still  further  augmenting  its  blood-content.  The 
rhythm  of  the  auricular  waves  is  fairly  constant,  but  in  poly- 
graph curves  is  somewhat  disturbed  by  carotid  waves  occurring 


200 


DISEASES  OF  THE  HEART 


approximate^  at  the  same  moment,  or  by  respiratory  move- 
ments of  the  sterno-mastoid  muscle.  If  measurements  are 
taken,  however,  at  corresponding  respiratory  phases  and  from 
points  which  are  not  coincident  with  carotid  beats,  the  number 
of  a  waves  in  stretches  of  equal  length  is  exactly  the  same. 
In  Figs.  117,  118,  119  the  waves  number  about  270  and  240 
per  minute. 


Fig.  117. — Cervical  Curve  rs  Auricular  Flutter,     (a. v. 


5  to  1.) 


The  rate  of  the  auricular  contractions  is  generally  in  the 
neighbourhood  of  300,  and  the  highest  record  is  350.  Ritchie's 
Case  5  suggests  that  thej^  may  reach  454. 

Tlie  rate  and  rhythm  of  the  ventricular  contractions,  on 
the  other  hand,  vary  within  very  large  limits.  In  Fig.  116 
the}'  number  72,  the  A.V.  ratio  being  regularly  4  to  1.  In 
Figs.  117,  118,  119  they  number  54-5,  60,  and  120  per  minute, 
the  A.V.  ratios  being  5  to  1,  4  to  1,  2  to  1.  The  cervical 
curves  are  most  easilj'  deciphered  in  Fig.  117.     In  this  figure 


a-:  7.tfO.      v  :  6o 

Fig.  118. — Cervical  Curve  in  Auricular  Flutter.     {a.v.  =  4  to  1.) 

each  cardiac  cycle  is  represented  by  fi^ve  waves,  the  largest  of 
which  is  evidently  synchronous  with  the  carotid  pulse.  The 
succeeding  wave,  however,  is  almost  as  great,  and  can  only  be 
partly  due  to  v  ;  and  an  evident  auricular  wave  a  precedes 
each  carotid  elevation.  The  intermediate  waves  occur,  as  is 
evident  on  reference  to  the  radial  pulse,  during  the  diastole 
of  the  ventricle,  and  are  of  equal  duration  and  of  the  same 


AURICULAR  FLUTTER 


201 


length  as  a,  and  the  period  c-c  is  five  times  the  length  of  a. 
Each  wave,  then,  is  in  part  or  in  whole  the  result  of  a  regularh' 
recurring  auricular  contraction,  and  the  auricles  are  contract- 
ing five  times  as  often  as  the  ventricles .  In  Fig  .118  the  cardiac 
cycle  shows  four  waves  which,  b}'  the  same  argument,  are  also, 
in  whole  or  in  part,  of  auricular  origin,  but  the  A.V.  ratio  is 
4  to  1.  In  Fig.  119  only  two  waves  are  present  in  the  cervical 
curve,  but  as  the  largest  wave  coincides  mth  v  and  not  -^nth  c, 
it  is  eviclentlv  only  in  part  the  result  of  ventricular  contraction ; 
and  as  the  radial  pulse-rate  is  exactly  double  that  of  the 
preceding  figure,  it  is  clear  that  each  represents  in  part  an 
auricular  contraction,  the  A.V.  ratio  being  2  to  1. 

The  ventricular  contractions,  however,  are  not  necessarily 
always  regular.  In  Fig.  120  the  first  two  and  the  last  ^our 
pulse  periods  are  of 
equal  length,  but  the 
intervening  periods  are 
all  shorter  and  varj^  in 
duration,  though  four 
in  series  are  in  one  place 
equal.  On  examination 
of  the  cervical  curve 
the  number  of  the  waves 

between  successive  carotid  beats  is  found  to  varj-,  the  series 
being  4,  4,  2,  2,  3,  2,  2,  2,  2,  1,  2,  4,  4,  4,  4;  but  as  each 
carotid  wave  evidently  overlaps  an  auricular  wave,  the 
series  of  auricular  contractions  is  evidently  5,  5,  3,  3,  4,  3,  3,  3, 
3,  2,  3,  5,  5,  5,  5,  and  the  ventricles  are  either  responding  to 
every  second,  third,  fourth,  or  fifth  auricular  contraction, 
or  contracting  independenth-  of  the  auricles.  The  ventricular 
electric  complex  in  Fig.  116  is  of  normal  character  so  far  as 
can  be  seen,  which  indicates  that  the  contraction  is  originating 
near  the  auriculo -ventricular  junction.  In  Ritchie's  first  case 
full  heart-block  was  present,  and  the  ventricular  contractions 
were  quite  regular,  with  a  pulse-rate  of  30  to  40  per  minute, 
the  usual  idiopathic  ventricular  rate.  But  in  Fig.  120  the 
ventricular  contractions  are  never  less  than  50,  a  figure 
greater  than  those  which  occur  in  cases  of  full  heart-block,  so 
that  the  latter  condition  mav  be  excluded.     A  partial  heart 


Fig. 


119.  —  Cervical    Cukve    in    Auricular 
Flutter,     (a. v.  =  2  to  1.) 


202  DISEASES  OF  THE  HEART 

block  may  occur  in  cases  of  sinus  rhythm,  and  a  partial  block 
seems  the  probable  explanation  of  the  varying  pulse-rate  in 
auricular  flutter.  The  most  common  A.V.  ratios  seem  to  be 
2-1  and  4-1,  and  an  abrupt  change  from  one  to  the  other  may 
double  or  halve  the  pulse-rate  instantaneously. 

The  arterial  curves  show  as  a  rule  a  characteristic  appearance, 
and  can  generally  be  distinguished  from  those  of  auricular 
fibrillation.  The  pulse  periods  in  the  latter  are  totally 
irregular,  and  occur  without  any  recognizable  sequence,  or 
definite  relationship  between  individual  beats.  In  auricular 
flutter,  on  the  other  hand,  series  of  rhythmic  ventricular  beats 
occur  at  times  (Fig.  121),  and  the  periods  of  an  irregular  rhj^thm 
tend  to  recur  and  to  bear  a  deflnite  relationship  to  each  other. 
The  two  longer  pulse  periods  in  Fig.  122  are  thus^ equal,  and 


Fig.   123.  —  Brachial   Curve   in   Auricular    Flutter. 
The  underlined  groups  of  beats  are  of  equal  duration. 

bear  to  the  intervening  beats  the  ratio  7  to  6.  In  Fig.  120 
the  correspondence  is  less  close.  A  premature  ventricular 
systole  is  accompanied  by  a  prolongation  of  both  the  presphyg- 
mic  interval  and  the  transmission  time,  and  the  arteiial  wave 
is,  in  consequence,  separated  from  its  precursor  by  a  longer 
interval  than  obtains  between  the  ventricular  contractions,  as 
shown  on  the  apex  tracing  (c/.  Fig.  80).  If  the  ventricular 
contraction  is  delayed,  the  presphygmic  and  transmission 
periods  are  shortened,  and  the  pulse  period  is  then  shortened 
as  weU. 

Comparable  stretches  may,  however,  be  found  if  care  be 
taken  to  contrast  stretches  which  are  preceded  and  ended  by 
equal  pulse  periods  (Fig.  123),  so  that  the  transmission  time 
and  presphygmic  period  are  equal  in  the  two  cases.  In 
Fig.  121  five  beats  of  the  frequent  rate  exactly  equal  three  of 
the  infrequent  rate. 


Five 


slow  rhvthm. 


iTo  face  paffe  2.02. 


3  3  3  3-3 

Fig.  120. — Cervical  Cfrve  in  Auricular  Flutter. 
The  A.V.  ratio  is  incoiatant. 


Fig.  121. — Brachial  Curve  in  Auricular  Flutter, 
Five  pulse  periods  of  the  frequent  rhythm  equal  three  pulse  periods  of  the  slow  rhythn: 


AJUU 


Fig.  122.— Cervical  Curve  in  Auricular  Flutter. 
The  two  longer  pulse  periods  are  equal. 


AURICULAR  FLUTTER  203 

Auricular  flutter  has  been  recognized  for  too  short  a  time 
to  enable  any  definite  conclusion  to  be  stated  with  regard  to 
its  significance,  but  it  is  already  evident  that  it  may  occur 
under  various  conditions,  and  it  has  been  found  in  acute  and 
chronic  valvular  disease,  in  hearts  that  are  enlarged  and  evi- 
dently degenerate,  and  in  hearts  that  are  of  normal  size  and 
probably  healthy.  It  may  arise  and  continue  for  varying 
intervals,  hours,  days,  and  certainly  weeks,  and  may  cease  and 
recur  from  time  to  time.  In  some  cases  it  has  been  succeeded 
by  auricular  fibrillation;  in  others  by  a  normal  rhythm,  and 
the  transition  may  be  extremely  abrupt. 

The  symptoms  that  are  met  with  in  auricular  flutter  are 
often  subjective  rather  than  objective.  This  seems  to  be  due 
to  the  fact  that  it  occurs  in  patients  whose  cardiac  reserve  is 
ample  as  well  as  in  those  who  are  already  suffering  from  cardiac 
insufficiency;  and  while  in  the  former  its  appearance  is  of 
■comparatively  Mttle  significance  if  the  paroxysms  are  of  short 
duration,  in  the  latter  its  onset  rapidly  induces  extreme  failure. 

There  is  little  doubt  that  auricular  flutter  is  not  uncommon, 
though  the  number  of  cases  that  have  been  reported  is  still 
small,  but  many  patients  whose  auricles  are  probably  fluttering 
a.re  too  ill  to  allow  a  detailed  examination,  and  the  recorded 
cases  are  thus  the  less  serious,  and  the  prognosis  on  the  avail- 
able data  is,  in  consequence,  erroneous. 

The  cases  which  are  narrated  below  illustrate  this  point. 
In  the  first  the  objective  signs  of  cardiac  failure  were  slight,  in 
the  second  severe,  and  in  the  third  completely  absent. 

Case  1. — A  shipyard  labourer,  aged  fifty-one,  was  admitted 
into  my  wards  complaining  of  palpitation,  shortness  of  breath, 
and  pain  in  the  epigastrium.  i 

The  symptoms  made  their  appearance  about  a  year  before 
his  admission,  when  he  first  became  conscious  of  his  heart's 
contractions.  At  the  outset  the  attacks  only  occurred  on 
severe  exertion,  and  ceased  shortly  after  he  stopped  work,  and 
they  were,  he  thought,  more  frequent  after  alcoholic  excess. 
He  was  short  of  breath  during  the  paroxysms,  and  often  giddy 
as  well,  but  he  never  fell  down.  During  the  last  few  months 
the  attacks  had  been  more  easily  induced  by  exertion,  and  the 
breathlessness  had  been  exaggerated,  and  for  three  weeks  he 


204  DISEx4SES  OF  THE  HEART 

had  had  a  constant  gnawing  pain  in  the  epigastrium.  The 
palpitation,  he  says,  is  a  frequent  action  of  the  heart,  "  Hke  a 
bird  fluttering,  with  occasional  irregular  thumps."  Ten  days 
before  admission,  after  a  bout  of  drinking,  it  became  constant, 
and  did  not  remit  during  rest.  The  pain  in  the  epigastrium 
was  constant,  not  related  to  the  ingestion  of  food,  and  steadily 
became  more  severe,  and  he  was  forced  to  cease  work  five 
days  after  the  onset  of  the  attack.  He  felt  very  weak  and. 
ill,  and  was  only  able  to  reach  the  hospital  with  the  greatest 
difficulty,  though  he  quickly  rallied  after  being  put  to  bed. 

He  was  a  big,  muscular  man,  and  lay  easily  in  bed  with  two 
pillows.  The  respirations  were  somewhat  frequent  (36  to  42)' 
and  irregular,  and  at  times  sighing  in  character.  There  was 
no  oedema,  but  the  liver  was  large  and  somewhat  tender.  The 
other  viscera,  save  the  heart,  appeared  normal,  but  the  urine 
contained  a  fair  quantity  of  albumin. 

The  apex  impulse  was  indistinct  and  badly  sustained,  and 
was  situated  in  the  fifth  interspace  in  the  nipple  Une.  The- 
area  of  cardiac  cluhiess  measured  5|  inches  transversely,  both 
sides  of  the  heart  being  slightly  dilated.  The  sounds  were- 
muffled  and  indistinct,  but  pure.  The  second  sounds  at  the- 
base  were  emphatic,  the  emphasis  being  on  the  pulmonic 
element.  The  cardiac  action  was  frequent,  numbering  136  tO' 
150,  and  extremelj^  irregular,  little  runs  of  five  to  twenty  beats 
of  even  rhj^thm  and  force  being  separated  from  each  other  by 
pauses  of  slightly  longer  duration,  or  by  runs  of  beats  at  a  less 
frequent  rate.     The  pulse  w^as  of  good  volume,  but  soft. 

His  condition  remained  unchanged  for  forty-eight  hours 
after  admission,  during  which  he  took  his  food  fairly  well  and 
slept  for  reasonable  periods,  being  apparently  comfortable- 
when  at  rest,  but  very  breathless  and  weak  on  even  trivial 
exertion  (stool,  etc.).  Between  midnight  and  2  a.m.,  however, 
the  cardiac  action  suddenly  altered,  the  pulse-rate  falling  ta 
80,  and  the  rhythm  becoming  perfectly  regular.  The  patient 
was  conscious  of  his  improvement  and  of  the  cessation  of  the 
flutter.  His  progress  afterwards  was  good.  The  pulse  re- 
mained infrequent  and  regular,  save  for  a  few  ventricular 
extra-systoles  which  were  noticed  in  the  succeeding  twenty- 
four  hours  ;  the  area  of  cardiac  clulness  rapidly  diminished  to 


AURICULAR  FLUTTER  205 

4J  inches,  and  the  hepatic  engorgement  and  pain  passed 
away. 

The  habits  of  this  patient  were  unsatisfactory  in  every  way- 
He  drank  and  smoked  heavity,  and  was  engaged  in  arduous 
manual  labour,  circumstances  which  seemed  to  be  the  chief 
cause  of  his  cardiac  disabilities. 

Case  2. — ^A  wire-drawer,  aged  sixty-one,  was  admitted  to 
my  wards  on  April  5,  complaining  of  shortness  of  breath  and 
swelling  of  the  feet  a  nd  legs . 

He  had  been  a  healthy  man  until  the  preceding  December, 
save  for  an  attack  of  dropsy,  which  only  lasted  for  a  few  days, 
three  years  before.  His  early  symptoms  consisted  of  a  feeling 
of  sickness  after  taking  food,  accompanied  by  giddiness,  but 
he  continued  at  his  work  until  he  caught  cold  early  in  January. 
At  this  time  he  had  a  harassing  cough  and  spit,  accompanied 
by  pain  in  the  chest,  and  he  was  forced  to  take  to  bed.  He 
was  very  breathless  and  had  paroxysms  of  dyspnoea  at  night, 
which  lasted  for  about  haK  an  hour.  A  few  days  after  he  went 
to  bed  his  feet  began  to  swell.  After  nine  days  the  symptoms 
subsided,  and  he  was  able  to  resume  work;  but  he  felt  weak 
and  ill,  and  became  breathless  on  slight  exertion.  The  oedema 
was  always  greater  at  night  after  his  work,  and  the  paroxysms 
of  dyspnoea  still  continued.  He  was  giddy  at  times,  particu- 
larly when  at  work,  and  as  all  the  symptoms  increased,  he 
sought  admission  to  hospital. 

He  was  a  badly  nourished  man  of  poor  physique,  and  re- 
quired to  be  propped  up  in  bed  on  account  of  shortness  of 
breath.  Qi]clema  was  well  marked  and  extended  on  to  the 
trunk.  The  chest  was  barrel-shaped,  and  there  was  wide- 
spread catarrh  of  the  lungs,  with  rales  at  the  bases.  The  hver 
was  enlarged,  but  was  not  tender.  The  left  heart  was  enlarged, 
the  apex  impulse  being  felt  in  the  nipple  line  in  the  fifth  space. 
Double  aortic  murmurs  were  audible  over  the  sternum;  the 
second  aortic  sound  was  inaudible.  The  arteries  were  very 
hard  and  tortuous,  and  the  pulse  numbered  90,  and  was 
regular  and  notably  shotty.  The  urine  contained  a  trace  of 
albumin.  The  knee-jerks  were  slight,  but  equal;  the  pupil- 
lary reactions  were  trivial;  and  the  Wassermann  test  was 
frankly  positive.     His   symptoms   rapidly   subsided,    and   he 


206  DISEASES  OF  THE  HEART 

left  hospital  a  week  later  of  his  own  accord,  though  the  oedema 
was  still  present.  A  week  later  he  resumed  work,  but  he  was 
never  able  to  do  a  full  day's  darg,  as  the  slightest  exertion  made 
him  very  breathless.  A  few  weeks  afterwards  the  cough 
returned,  and  all  his  symptoms  became  exaggerated.  The 
nocturnal  dj'spnoea  reappeared,  and  he  had  again  to  be  propped 
up  in  bed,  and  he  slept  badly  and  the  oedema  steadily  increased. 
He  was  readmitted  to  hospital  on  May  23.  He  now  looked  ill 
and  collapsed,  and  was  in  full  orthopnoea.  The  oedema  again 
invaded  the  trunk;  the  bases  of  the  lungs  were  congested,  and 
the  liver  was  enlarged  and  tender.  The  respirations  were 
shallow  and  frequent,  and  slightly  irregular.  The  heart  was 
a  little  larger  than  on  his  previous  residence,  pulsation  being 
apparent  in  the  sixth  interspace.  The  rate  was  very  frequent 
(about  150),  but  the  rhythm  was  quite  regular.  The  systohc 
aortic  murmur  was  still  distinct,  but  the  second  sound  was 
closed,  the  diastolic  murmur  having  disappeared.  The  pulse 
was  fairly  full  and  still  shotty. 

After  his  admission  his  symptoms  steadily  impioved.  The 
urinary  output  became  ample,  and  the  oedema  diminished 
and  the  orthopnoea  became  less  marked.  A  pulmonary  infarct 
occurred  on  May  27,  but  this  did  not  interfere  with  his  progress. 

The  frequent  cardiac  action,  however,  continued  until  June  3, 
the  rate  varying  between  140  and  178;  but  on  that  morning, 
between  6  a.m.  and  8  a.m.,  it  suddenly  fell  to  92,  and  after- 
wards to  76.  It  was  now  notably  irregular  from  auricular  fibrilla- 
tion. At  2  p.m.  on  June  4  the  rhythm  again  altered,  and  the 
pulse  became  quite  regular,  but  very  frequent  (140  to  174). 
This  continued  until  8  a.m.  on  June  5,  when  the  rate  again  fell 
suddenly  to  88.  The  rhj'thm  was  now  quite  regular,  save  for 
the  presence  of  an  occasional  extra-systole,  which  was  appar- 
ently always  ventricular  in  origin. 

There  are  several  points  of  interest  in  the  case.  The  patient 
was  never  conscious  of  the  cardiac  action,  and  was  unable  to 
state  whether  the  tachycardia  had  occurred  prior  to  his  second 
admission,  or  the  time  of  its  onset.  He  was  given  60  minims  of 
tinct.  cligitaHs  daily  at  first,  a  week  later  75  minims,  and  two 
days  later  (June  1),  90  minims,  and  with  apparent  benefit, 
though  there  was  no  change  in  the  pulse-rate. 


AURICULAR  FLUTTER  207 

Cervical  tracings  were  frequently  obtained  during  the  period 
of  tachycardia.  The  a  wave  was  always  distinct,  and  preceded 
the  c  by  O'lO  second,  while  v  occurred  early,  and  filled  up  the 
rest  of  the  curve.  Two  interpretations  are  possible:  a 
"nodal  "  tachycardia  or  a  2-1  auricular  flutter,  every  other 
auricular  contraction  being  hidden  beneath  the  c-v  waves; 
and  as  the  paroxysm  passed  into  undoubted  auricular  fibrilla- 
tion, the  second  explanation  seems  the  more  probable.  No 
tracings  were  obtained  during  the  second  paroxysm,  which  was 
succeeded  by  a  normal  rhythm. 

The  disappearance  of  the  diastolic  aortic  murmur  during  the 
tachycardia  was  presumably  due  to  the  shortness  of  diastole, 
which  did  not  permit  sufficient  regurgitation  to  produce  audible 
vibrations,  and  the  murmur  reappeared  as  soon  as  the  rate 
became  sufficiently  slow  and  diastole  lengthened.  The  pulse 
altered  considerably  in  volume  with  the  change  in  rate, 
and  became  larger  with  the  less  frequent  beats ;  but  it  varied 
httle  in  force,  the  systolic  pressure  only  varying  between  145 
and  152  mm.  during  the  periods  of  tachycardia  and  fibrillation, 
though  it  fell  to  130  mm.  when  the  regular  rhythm  reappeared. 
This  fall,  however,  accompanied  the  disappearance  of  the 
oedema,  and  the  higher  levels  may  have  been  due  to  its  presence. 

The  beneficial  action  of  digitalis  was  clearly  shown  by  the 
lessening  of  the  dyspnoea  and  the  oedema,  and  the  increase  of 
the  urinary  output;  but  the  improvement  occurred  without 
any  reduction  of  the  pulse-rate — a  most  unusual  occurrence. 
James  Mackenzie  has  described  the  occurrence  of  fibrillation 
following  flutter  on  the  administration  of  full  doses  of  digitahs, 
but  this  is  the  only  example  of  the  sequel  which  has  come  under 
my  own  observation. 

Case  3. — Another  patient,  a  lad  of  seventeen,  who  com- 
plained of  palpitation,  dated  his  attacks  from  a  fright  which 
he  had  received  at  the  age  of  twelve  on  being  chased  by  a 
drunken  man.  Two  months  before  his  admission  to  hospital 
he  slid  for  12  feet  down  a  ladder,  and,  though  merely  bruised, 
was  greatly  frightened.  The  attacks  of  palpitation  became 
more  frequent,  and  he  became  very  breathless  on  exertion, 
and  easily  tired.  He  was  a  very  nervous  boy,  and  was  anxious 
about  his  condition,  as  his  previous  health  had  not  been  good 


208  DISEASES  OF  THE  HEART 

He  had  suffered  from  growing-pains  when  at  school,  and  had 
had  his  right  arm  broken  by  an  accident ;  and  enlarged  glands 
had  been  removed  from  the  left  side  of  his  neck  at  the  age  of 
nine.  The  scars  were  sound,  but  the  wounds  had  evidently 
been  deep ;  they  ran  downwards  from  the  angle  of  the  jaw  to 
the  thyroid  cartilage,  and  the  vagus  nerve  might  well  have 
been  nipped  in  the  cicatrix. 

The  pulse  was  extremely  unstable,  varying  between  60  and 
214,  and  the  beats  were  sometimes  in  twins  or  triplets  even  on 
the  same  day.  The  tachycardia  commenced  and  ended 
abruptly,  and  the  paroxysms  lasted  for  varying  periods — a 
minute  or  two,  or  twenty-four  hours — but  they  generally  ceased 
more  or  less  completely  during  sleep,  and  were  intensified  during 
examination.  He  complained  of  discomfort  in  the  cardiac 
region  during  their  continuance,  and  sweated  profusely,  and 
breathed  heavily,  but  he  lay  comfortably  flat  in  bed.  When 
the  pulse-rate  was  frequent,  the  right  heart  and  the  liver  be- 
came enlarged,  but  they  rapidly  regained  their  normal  size 
when  the  paroxysms  ceased.  A  mitral  sj^stohc  murmur  was 
present  on  his  first  admission,  but  a  year  later  the  cardiac 
sounds  were  pure  and  the  heart  was  of  normal  size,  so  that 
the  incompetence  was  probably  functional.  The  attacks  at 
this  time  were  much  less  frequent,  and  none  occurred  during 
a  week's  residence  in  hospital . 

Tracings  were  obtained  on  many  occasions.  In  one,  when 
the  pulse  numbered  214  per  minute,  the  a-c  interval  measured 
less  than  O'lO  second  (Fig.  115).  At  other  times,  however, 
the  auricles  passed  into  flutter,  and  the  pulse  became  extra- 
ordinarily mobile  (Fig.  120).  On  these  occasions  a  bigeminal 
or  a  trigeminal  rhythm  might  be  maintained  for  several  seconds 
or  minutes. 

When  the  auricles  were  fluttering,  the  pulse-rate  was  curi- 
ously mobile,  the  records  taken  at  about  hourly  intervals  one 
day  numbering  156,  214,  168,  128,  108,  100,  128  (120,  128,  116, 
80,  84,  80,  76,  90,  while  he  was  sleeping),  104,  112,  64,  196, 
224,  168.     The  condition  persisted  for  nearly  three  months. 

The  case  is  interesting  on  account  of  the  neurotic  character 
of  the  patient.  The  symptoms  succeeded  a  fright ;  the  pulse- 
rate  was  always  increased  by  examination  and  lessened  when 


AURICULAR  FLUTTER  209 

he  was  asleep,  and  the  patient  was  extremely  excitable. 
Digitalis,  opium,  tinct.  belladonnse,  vagal  pressure,  etc.,  seemed 
to  have  little  influence,  and  a  watchful  neglect  appeared  to 
be  the  most  useful  therapeutic  measure.  The  subsequent 
course  of  events  confirmed  the  impression  that  the  cause  of 
the  attacks  was  probably  situated  outside  the  heart. 

The  depth  of  the  cervical  scars  suggested  the  possibility  of 
irritation  of  the  vagus  nerve,  but  pressure  upon  the  other  vagus 
and  the  administration  of  belladonna  seemed  to  have  no  effect 
upon  the  cardiac  action.  Ritchie's  Case  4  also  suffered  from 
enlarged  glands  and  sinuses  in  the  neck. 

The  papers  of  Ritchie  and  Lewis  contain  reports  of  23  cases, 
to  which  I  have  added  7  of  my  own,  in  which  the  polj^graphic 
records  seem  clear.  Of  these  patients  24  were  males  and 
6  were  females  ;*  21  were  over  forty  years  of  age,  the  youngest 
patient  being  aged  fourteen  and  the  oldest  seventy-four; 
3  suffered  from  disease  of  the  aortic  (in  2  cases  of  acute  char- 
acter), and  9  from  disease  of  the  mitral  valve,  and  1  from 
adherent  pericardium;  5  patients  had  a  high  blood-pressure; 
9  complained  chiefly  of  paroxysms  of  tachycardia;  in  3  at 
least  the  heart  was  probably  normal;  in  1  case  the  flutter 
developed  and  ceased  during  an  operation  for  osteomyelitis. 

In  Ritchie's  Case  1,  flutter  has  lasted  almost  continuously  for 
seven  years.  Thirteen  cases  passed  at  one  time  or  another 
into  auricular  fibrillation. 

Only  2  cases  are  reported  as  having  died  under  observa- 
tion, while  1  was  moribund  when  last  seen.  The  records, 
Jiowever,  on  this  point  are  insufficient,  and  the  true  mortality 
is  probably,  as  akeady  mentioned,  greater  than  would  appear. 
The  prognosis  in  an  individual  case  depends  upon  several 
factors,  the  most  important  being,  as  akeady  mentioned,  the 
■degree  of  the  cardiac  reserve.     The  frequency  and  the  (Juration 


Age. 

Cases. 

*  10  to  19  years 

..     4 

20  „  29      „ 

..     2 

30  „  39     „ 

..     3 

40  „  49      „ 

..     6 

50  „  59     „ 

..     6 

60  „  69      „ 

..     6 

70  „  79     „ 

..     3 

14 


210  DISEASES  OF  THE  HEART 

of  the  paroxysms,  their  relation  to  removable  causes  (alcohol, 
tobacco,  etc.),  are  also  important.  In  Ritchie's  Case  1  full 
heart-block  was  present,  and  the  ventricular  action  was  in- 
frequent and  regular.  The  block  was  in  all  probabihty  useful, 
as  it  prevented  undue  frequency  of  the  ventricular  contractions, 
and  my  observations  point  to  the  conclusion  that  rapid  ven- 
tricular contractions  lead  much  more  quickly  to  cardiac  failure 
than  rapidity  of  the  auricular  contractions  accompanied  by  a 
moderate  ventricular  rate.  The  same  conclusion  probably 
apphes  to  auricular  fibrillation.  The  occurrence  of  auricular 
flutter  in  acute  endocarditis  is  not  necessarily  followed  by  per- 
manent irregularity-  of  the  cardiac  action,  for  in  one  case  in 
which  it  arose  and  persisted  for  at  least  ten  days  under  my 
observation,  the  cardiac  rhythm  was  quite  normal  two  years, 
later.     The  flutter  had  not  recurred  in  the  interval. 

Treatment. — James  Mackenzie  states  that  auricular  fibrilla- 
tion may  be  induced  in  flutter  by  full  doses  of  digitalis,  and  that 
if  the  drug  be  then  intermitted  a  normal  rhythm  may  ensue. 
A  similar  sequence  has  been  observed  by  Lewis  and  by  myself, 
and  this  treatment  by  digitalis  should  be  pursued  whenever 
the  disturbance  is  recognized ;  but  it  is  not  invariably  success- 
ful, and  has  failed  in  some  cases.  In  one  of  my  cases,  too,  the 
auricular  fibrillation  continued  until  the  patient's  dismissal, 
though  her  general  condition  improved  very  greatly. 

The  administration  of  digitalis  is,  moreover,  only  a  part  of 
a  rational  treatment,  and  aU  the  other  measures  indicated  in 
cardiac  failure  should  be  carried  out — in  particular,  absolute 
mental  and  physical  rest. 


CHAPTER  XVII 
AURICULAR  FIBRILLATION 

In  many  forms  of  cardiac  disease,  and  particularly  in  mitral 
stenosis,  the  pulse  is  notably  irregular  in  rhythm  for  long 
periods  of  time.  The  condition  has  been  known  for  many 
years,  and  has  been  called  the  "mitral  pulse,"  "  dehrium 
cordis,"  "pulsus  irregularis  perpetuus,"  etc.,  by  various 
writers ;  but  its  cause,  until  recently,  remained  obscure.  In 
1906,  however,  Cushny  and  Edmunds  pointed  out  the  close 
resemblance  of  this  irregular  pulse  to  that  which  occurs  in 
animals  whose  auricles  are  fibrillating,  and  suggested  that  it 
might  be  due  to  the  same  cause.  In  1907  James  Mackenzie 
formulated  the  same  theory  as  a  result  of  his  investigations  of 
the  venous  pulse,  though  later  on  he  attributed  this  irregularity 
to  other  causes.  In  1909  Rothberger  and  Winterberg,*  using 
the  electro-cardiograph,  brought  forward  strong  evidence  in 
favour  of  Cushny  and  Edmunds'  conclusions,  and  the  indepen- 
dent work  of  Lewis, t  and  Jolly  and  Ritchie, J  using  similar 
methods,  has  placed  the  association  beyond  doubt,  the  cervical 
and  electrical  curves  in  dehrium  cordis  being  exactly  similar 
to  those  obtained  from  animals  whose  auricles  are  fibrillating. 

Auricular  fibrillation  is  easily  produced  in  animals.  It 
occurs  frequently  in  the  dying  heart,  and  follows  faradic 
stimulation  of  the  auricles,  ligature  of  a  coronary  artery, 
and  the  administration  of  various  drugs  (potassium  bromide, 
adrenalin,  etc.).  When  fibrillation  ensues,  the  normal  co- 
ordinate contraction  of  the  auricle  as  a  whole  ceases,  and 
the  chamber  dilates;  the  muscular  fibres  contract  in  little 
bundles  here  and  there,  so  that  the  surface  is  in  a  state  of  per- 

*  Wien.  Iclin.  Wochenschr.,  1909,  vol.  xxii.,  p.  839. 
■\  Heart,  1909-10,  vol.  i.,  p.  306. 
t  Ibid.,  1910-11,  vol.  ii.,  p.  177. 
211 


212 


DISEASES  OF   THE  HEART 


petual  quivering  or  flickering,  very  similar  to  that  wliicli  may 
be  seen  in  the  tongue  and  systemic  muscles  (fibrillation)  in 
cases  of  progressive  muscular  atrophy.  The  ventricular  con- 
tractions remain  co-ordinate,  but  their  rhythm  is  disturbed, 
and  the  beats  are  notably  irregular.  Auricular  fibrillation  is 
often  permanent  when  once  it  has  ensued,  and  continues  until 
the  heart  ceases  to  beat;  but  it  may  stop  and  the  normal 
sequence  of  contractions  may  reappear  if  the  stimulus  is 
removed  and  the  vagus  nerve  strongly  stimulated,  or  if  the 
heart  is  perfused  with  a  suitable  fluid. 

The  yulse  in  auricular  fibrillation  is  very  characteristic,  the 
beats  being  wholly  irregular  in  their  sequence  and  their  size. 


Fig.  124. — The  Radial  Pulse  in  Auricular  Fib  rill  ateon'. 


The  varying  size  of  the  waves  is  extremely  striking,  and  is 
not  dependent  upon  the  duration  of  the  preceding  diastole  as 
in  a  normal  heart-beat,  but  may  be  now  large  and  now  small, 
though  the  pulse  periods  are  nearly  equal  (Fig.  124). 

The  cervical  curve  is  equally  distinctive.  If  the  pulse-rate 
is  frequent,  it  usually  shows  a  single  large  wave,  perhaps 
broken  up  into  two  or  more  summits,  commencing  synchron- 
ously with  the  carotid  beat  (Fig.  125).  The  a  wave  has  dis- 
appeared from  its  usual  situation  immediately  before  c,  and  the 
X  depression  is  also  ab-^ent.  The  v  wave  may  "  anticipate  " 
and  succeed  c  without  any  interval,  or  may  be  separated  from 
it  by  an  interval  of  short  duration.  If  the  pulse-rate  is  infre- 
quent, a  new  series  of  waves  may  be  recognized  during  the 


AURICULAR  FIBRILLATION 


213 


fe 


diastole  (Figs.  125,  126).  These  are  generally  smaU  and  of 
varying  size  and  duration,  numbering  from  300  to  600  per 
minute;  but  accurate  enumeration  is  impossible,  as  some  of 
the   wavelets   are   lost  when  c  and  v     l  ^  i 

supervene.  The  wavelets  may  be  quite 
distinct  in  the  apex  tracing,  and  the  a 
wave  is  always  absent  both  here  and 
in  the  liver  tracing. 

Electro-cardiographic  curves  show  a 
comparable  curve  (Fig.  71).  The  normal 
P  wave  has  disappeared,  and  ventricu- 
lar diastole  is  occupied  by  a  series  of 
tiny  deflexions  exactly  similar  to  those 
that  are  found  in  the  cervical  curves. 
The  ventricular  complex  is  normal. 

The  rate  of  the  pulse  varies  within 
large  limits.  It  is  often  about  normal, 
and  in  this  case  symptoms  of  cardiac 
weakness  are  usually  trivial  or  in  abey- 
ance; it  may  be  greatly  increased, 
running  about  120  or  even  as  high  as 
160,  and  then  symptoms  of  cardiac 
weakness  are  generally  apparent ;  vevy 
rarely  it  is  infrequent,  numbering  about 
30,  or  even  less. 

There  has  been  considerable  dis- 
cussion as  to  the  site  of  origin  of  the 
stimuli  which  produce  the  ventricular 
systoles,  for  it  is  conceivable  that  the 
ventricles  may  follow  their  own  intrinsic 
rhythm,  or  may  respond  to  some  of  the 
stimuli  which  are  continually^  being 
showered  upon  them  by  the  auricles ; 
but  it  seems  certain  that  the  'latter 
conception  applies  to  most  cases.  An  intrinsic  ventricular 
rhythm  is  infrequent  and  regular,  the  pulse  numbering  about 
30  beats  per  minute,  the  antithesis  of  that  in  most  cases  of 
auricular  fibrillation ;  the  ventricular  electric  complex  is  normal, 
so  that  the  ventricles  are  responding  to  stimuli  passing  to  it 


o 


214 


DISEASES  OF  THE  HEART 


•^ 


i 


i 


along  their  usual  route ;  and  the  a.v.]node  and  bundle  may  be 
normal  on  histological  examination  (Monckeberg,  Koch,  A.  M. 
Kennedy),  so  that  the  usual  pathway 
of  the  stimuli  is  intact  and  available. 

In  a  few  cases,  however,  the  ventri- 
cles have  been  shown  to  follow  their 
own  intrinsic  rhythm,  presumably  from 
accompanying  heart-block.  Lewis  and 
James  Mackenzie  have  recorded  cases 
in  which  the  ventricular  rate  was 
generally  infrequent  and  regular,  though 
auricular  fibrillation  was  demonstrated 
by  the  electro-cardiograph,  and  in  which 
premature  ventricular  contractions  were 
foUowed  by  a  pulse  period  of  normal 
length,  a  characteristic  feature  of  a 
ventricular  rhythm,  Fredericq  too  has 
severed  the  a.v.  bundle  experimentally 
in  animals  whose  auricles  were  fibrilla- 
ting,  and  has  recorded  the  occurrence 
of  a  regular  infrequent  ventricular 
beat.  It  seems  probable  that  minor 
degrees  of  defective  conduction  may 
also  occur,  and  impress  their  own  special 
characters  upon  the  pulse. 

The  onset  of  auricular  fibrillation  in 

experiment  seems  always  to  be  abrupt ; 

and  a  similar  onset  has  been  observed 

clinically    (James    Mackenzie),    cardiac 

symptoms  ensuing  abruptly,  and  being 

accompanied  by  notable  irregularity  of 

the  heart.     In  some  cases,  however,  the 

mode  of  onset  cannot  be  ascertained, 

as  the  patients  are  unconscious  of  the 

irregularity,   and  their  symptoms    are 

insidious  in  onset. 

The  duration  of  auricular  fibrillation  varies.     In  some  cases 

it  is  continuous,  and  it  may  be  present  for  years  in  persons 

who  are  enjoying  average  health.     In  others,   however,   its 


s   ^ 


AURICULAR  FIBRILLATION  215 

occurrence  is  the  signal  of  serious  symptoms,  and  life  may  be 
rapidly  endangered.  In  the  majority  of  cases,  when  once 
established,  it  is  permanently  present,  but  in  a  few  cases  it 
ceases  as  abruptly  as  it  begins,  after  a  period  of  varying 
duration,  the  paroxysms  lasting  for  minutes,  hours,  or  days. 

A  man  aged  forty-seven,  who  was  suffering  from  acute 
pneumonia,  had  two  attacks  of  auricular  fibrillation  under  my 
observation.  The  pulse,  though  frequent,  was  quite  regular 
until  the  morning  of  the  eighth  day,  when  quite  suddenly, 
about  3  a.m.,  it  presented  the  characteristic  irregularity,  the 
beats  numbering  about  120  per  minute.  This  continued  until 
11  p.m.,  when  it  again  became  quite  regular.  About  1  a.m. 
on  the  ninth  day  the  auricles  again  passed  into  fibrillation  for 
a  short  time,  but  subsequently  the  pulse  remained  regular,  and 
convalescence,  though  slow,  was  good.  SHght  oedema  of  the 
feet  ensued  for  a  few  days  after  he  got  up  out  of  bed,  but  this 
was  the  only  evidence  of  cardiac  weakness  throughout  the  ill- 
ness. 

In  exceptional  cases  its  occurrence  has  been  at  first  inter- 
mittent, but  ultimately  continuous. 

The  causes  of  auricular  fibrillation  are  at  present  unknown, 
but  several  considerations  may  be  borne  in  mind.  In  experi- 
ment auricular  fibrillation  may  be  produced  by  functional  dis- 
turbances {e.g.,  faradic  stimulation),  and  may  cease  when  the 
disturbing  factor  is  withdrawn.  From  the  clinical  standpoint 
the  cases  may  be  divided  into  two  groups :  one  in  which  it 
occurs  occasionally  and  in  paroxysms ;  and  another  in  which 
it  is  constantly  present,  perhaps  for  years ;  and  in  the  latter 
case  the  patient  may  enjoy  fair  health.  It  seems  probable 
that  the  cause  is  not  always  the  same.  One  can  hardly  con- 
ceive that  a  functional  disturbance  can  produce  an  effect  which 
continues  for  years,  or  that  a  functional  disturbance  can  be 
present  for  years  without  producing  very  obvious  symptoms . 

Auricular  fibrillation  occurs  in  many  forms  of  cardiac  dis- 
ease, but  is  particularly  common  in  mitral  stenosis  and  in 
hypertrophied  and  degenerate  hearts.  In  mitral  stenosis  the 
maximal  strain  is  laid  upon  the  left  auricle,  and  is  continuous, 
and  functional  disturbance  of  auricular  action  is  extremely 
likely  to  foUow.     In  mitral  disease  and  in  degenerate  hyper- 


216  DISEASES  OF  THE  HEART 

trophied  hearts  myocardial  fibrosis  is  often  present,  and  may 
involve  the  auricles  in  particular.  Pathological  observations 
are  stiU  scanty,  but  the  a.v.  node  and  bundle  have  been  found 
healthy  in  cases  of  auricular  fibrillation,  while  the  s.a.  node 
has  been  found  to  be  involved  in  an  inflammatory  focus  in  a 
case  where  auricular  contractions  took  place  regularly  during 
life  (Krumbhaar),  so  that  it  seems  improbable  that  the  irregu- 
larity is  produced  by  lesions  in  the  primitive  tissue.* 

Gaskell  has  suggested  that  fibrillar  contractions  may  be 
brought  about  by  a  blocking  in  the  connections  between  the 
branching  muscle  cells,  and  that,  in  consequence,  the  contrac- 
tions travel  at  different  rates  and  are  blocked  at  varying  dis- 
tances in  the  muscular  mass,  thus  giving  the  appearance  of 
inco-ordinate  contractions.  As  the  stimuli  are  weak  and  of 
var^ang  intensity,  ventricular  contractions  only  occur  occa- 
sionally whenever  maximal  stimuh  happen  to  reach  them. 

Disturbances  of  conduction  between  the  auricle  and  ven- 
tricle may  be  produced  by  functional  disturbance,  as  well  as 
by  organic  disease  of  the  a.v.  bundle,  and  functional  disturbance 
of  conduction  in  the  auricular  muscle  would  explain  paroxysmal 
fibrillation,  while  organic  disease  of  the  auricle  would  produce 
a  permanent  defect.  Further  chnical  and  pathological  observa- 
tions are  still  required  for  the  elucidation  of  the  problem,  but  it 
is  already  known  that  the  auricle  is  frequently  affected  by  a 
diffuse  (Fig.  14)  as  well  as  by  a  patchy  fibrosis. 

It  has  been  suggested  (Lewis)  that  auricular  fibrillation  is 
the  result  of  an  increased  excitability  of  the  auricular  muscle, 
whereby  ectopic  stimuli  are  constantly  arising  at  every  part 
of  the  wall.  It  can  be  reaclih'  produced  by  strong  faradization 
of  the  auricle;  its  occurrence  clinically  may  be  preceded  by  the 
appearance  of  auricular  extra-systoles ;  paroxysms  of  tachy- 
cardia of  auricular  origin  and  of  fibrillation  may  occur  in  the 
same  individual;  and,  as  already  mentioned,  inflammatory 
foci  are  often  present  in  the  auricular  wall.  But  the  failure 
of  vagus  stimulation  to  influence  auricular  fibrillation,  though 
it   undoubtedly   depresses    the    excitability   of    the   auricular 

*  In  14  cases  of  auricular  fibrillation  the  s.a.  node  was  normal  in  3,  the  a.v, 
node  in  9,  and  the  a.v.  bundle  in  8.  In  3  cases  all  three  were  normal.  (Cowan. 
Fleming,  and  Kennedy:  Trans.  Interna*.  Congiess,  1913.) 


AURICULAR  FIBRILLATION  217 

muccle  in  animal  experiments,  makes  GaskeU's  theory  the 
more  probable,  as  under  it  the  auricular  conductivity  would  be 
still  further  depressed  by  vagal  stimulation,  and  the  inco- 
ordinate action  of  the  auricle  would  be  intensified. 

In  the  majority  of  cases  auricular  fibrillation  is  first  recog- 
nized during  a  period  of  cardiac  insufficiency,  and  the  date  of 
its  onset  is,  in  consequence,  unknoTvoi.  As  a  rule,  its  occur- 
rence is  associated  mth  the  onset  of  defmite  sj^mptoms,  or,  at 
any  rate,  with  some  limitation  of  the  field  of  response ;  but  the 
severity  of  the  sjmiptoms  varies  considerably  in  different  cases, 
very  largely  in  correspondence  with  the  rate  of  the  ventricular 
contractions,  a  pulse-rate  of  140  being  accompanied  by  well- 
marked  evidences  of  failure,  while  a  pulse  of  normal  rate  may 
be  associated  with  but  few.  The  radial  pulse-rate  is  often 
misleading,  since  mam^  of  the  beats  may  be  missed,  and  the 
rate  should  be  ascertained  hj  auscultation 'or  by  palpation  of 
the  apex  impulse.  The  importance  of  this  factor  is  often  seen 
in  the  clinique,  a  patient  admitted  with  oedema,  orthopnoea,  etc., 
and  a  pulse  of  120  or  over,  losing  all  his  symptoms  coincidently 
with  a  reduction  of  the  pulse  to  70  or  its  neighbourhood, 
though  the  irregularity  persists  unchanged. 

It  is  in  mitral  stenosis  in  particular  that  auricular  fibrillation 
is  most  common.  In  this  lesion  the  strain  upon  the  left  auricle 
is  constant,  as  the  obstruction  at  the  mitral  valve  is  permanent, 
in  contrast  with  the  intermittent  strain  in  mitral  insufficiency 
where  the  auricular  congestion  is  rapidly  reheved  during 
ventricular  diastole.  The  cessation  of  co-ordinate  auricular 
contractions,  however,  makes  the  characteristic  crescendo 
murmur  disappear,  so  that  the  recognition  of  the  stenosis  is 
difficult,  unless  its  existence  is  already  known.  It  should, 
however,  be  suspected  if  a  systohc  murmur  is  present,  or  if 
the  second  sound  at  the  base  is  doubled,  or  the  second 
pulmonic  element  unduly  emphatic,  and  its  existence  may  be 
confidently  affirmed  if  the  apical  diastolic  murmur  is  recog- 
nized. 

In  auricular  fibrillation,  as  alreadj^  mentioned,  the  auricle 
dilates,  and  the  area  of  cardiac  clulness  is  altered  in  correspond- 
ing degree,  extending  outwards  to  the  right  as  far  as,  or 
beyond,  the  right  sternal  border. 


218  DISEASES  OF  THE  HEART 

The  murmurs  at  the  apex  in  auricular  fibrillation  are  ex- 
tremely variable,  and  are  often  impossible  to  define  in  cases 
where  the  cardiac  contractions  are  frequent;  for  in  this  case 
the  shortness  of  diastole  prevents  adequate  fiUing  of  the 
ventricle,  and  so  minimizes  systolic  reflux,  and  the  murmur 
may  only  be  audible  after  the  longer  pauses ;  while,  for  a  similar 
reason,  the  diastolic  murmur  may  also  fail.  Aortic  murmurs 
are  also  variable,  the  systolic  murmur  being  shorter  and  softer 
with  shortened  pulse  periods,  and  longer  and  harsher  after 
longer  intervals.  The  diastolic  murmur  may  be  unrecognizable 
if  the  pulse  is  very  frequent. 

The  prognosis  in  cases  where  auricular  fibrillation  has  ensued 
is  always  more  grave  than  in  comparable  cases  with  a  sinus 
rhythm,  and  I  have  never  seen  a  patient  with  this  condition 
whose  cardiac  power  was  not  at  any  rate  subjectively  lessened. 
James  Mackenzie  states  that  he  has  known  patients  lead 
arduous  lives  for  as  long  as  ten  years,  but  such  cases  are  cer- 
tainly exceptional.  One  of  my  patients,  who  died  at  the  age 
of  thirty-six,  had  persistent  auricular  fibrillation  for  at  least 
three  years  before  his  death,  and  enjoyed  fair  health  for 
months  at  a  time.  He  suffered  from  double  mitral  disease, 
and  the  first  symptoms  were  associated  with  a  pulmonary 
infarct. 

The  cases  which  are  associated  with  mitral  stenosis  seem  to 
have  a  better  prognosis  than  those  which  are  due  to  other 
cardiac  lesions.  In  mitral  stenosis  the  left  auricle  is  over- 
strained, and  its  action  is  perhaps  more  easily  disturbed.  In 
other  lesions  the  auricles  merely  share  in  the  general  stress, 
and  fibrillation  indicates  a  widespread  disorganization  of  the 
heart. 

In  a  general  way  the  inception  of  permanent  auricular 
fibrillation  is  the  beginning  of  the  end,  though  many  patients 
are  able  to  lead  quiet  fives  for  a  year  or  two  after  the  onset. 

The  dilatation  of  the  auricles,  which  always  ensues,  is  of 
particular  importance,  for  it  seems  to  be  a  main  factor  in 
producing  clotting  in  the  appendices,  and  the  strain  of  a 
pulmonary  infarct  is  badly  borne.  Infarcts  are  much  more 
common  than  is  perhaps  reahzed.  They  are  generally  accom- 
panied by  frank  haemoptysis  or  pleural  friction,  and  by  the 


AURICULAR  FIBRILLATION  219 

■evidences  of  consolidation;  but  I  have  often  found  more  in- 
farcts on  post-mortem  examination  than  were  suspected  from 
clinical  observation,  and  their  occurrence  need  not  be  accom- 
panied by  any  obvious  physical  sign.  A  central  infarct,  out- 
with  the  sphere  of  clinical  examination,  is  a  not  infrequent 
cause  of  the  onset  of  acute  cardiac  sj-mptoms. 

The  immediate  prognosis  seems  to  depend  chiefly,  if  not 
entirely,  upon  the  rate  of  the  ventricular  contractions,  and  upon 
the  response  to  the  administration  of  digitalis.  Patients  differ 
considerably  in  these  respects,  and  the  prognosis  is  better  if  the 
pulse,  with  or  without  drugging,  can  be  kept  within  normal 
limits.  One  of  Mackenzie's  cases  ^vith  heart-block  and  a 
regular  infrequent  pulse  was  working  regularly  two  years  later, 
^nd  a  degree  of  defective  conductivity  is,  in  all  probabihty, 
beneficial  rather  than  the  reverse.  The  case  which  I  have 
just  mentioned  seems  to  belong  to  this  category. 

In  many  patients  the  administration  of  digitahs  leads  to  a 
reduction  in  the  pulse-rate  and  to  the  disappearance  of  symp- 
toms, and  the  pulse  subsequently  remains  within  normal  rates. 
But  in  other  cases  the  drug  requires  to  be  administered  con- 
stantly, for  on  its  cessation  the  pulse  becomes  frequent  and 
the  symptoms  recur.  This  was  the  case  with  a  woman  at  one 
time  under  my  care,  who  stated  that  she  had  taken  digitalis 
constantly  for  seven  years.  Her  symptoms  rapidly  subsided 
upon  its  administration,  but  they  recurred  on  more  than  one 
■occasion  within  a  fortnight  of  its  being  stopped. 

The  treatment  of  auricular  fibrillation  is  mainly  a  matter 
■of  treatment  by  digitalis,  and  is  discussed  in  detail  in 
Chapter  XXVI.  The  drug  should  be  stopped  when  the  pulse 
numbers  60,  or  if  a  coupled  rhythm  supervenes. 


CHAPTER  XVIII 
ACUTE  ENDOCARDITIS 

The  clinical  distinction  between  simple  and  malignant  forms 
of  acute  endocarditis  is  apt  to  convey  an  erroneous  idea  of 
their  true  nature.  Both  are  due  to  bacterial  invasion,  and 
the  pathological  difference  is  merely  a  matter  of  degree,  the 
infection  in  the  one  case  being  readily  overcome,  and  in  the 
other  progressing  indefinitely ;  and  an  intermediate  group  con- 
nects the  links  at  each  end  of  the  chain.  The  difference  may 
be  due  to  several  causes  :  to  the  particular  variety  of  bacterium, 
to  its  virulence  or  its  dose,  or  to  the  resistance  of  the  tissues  tO' 
the  infection. 

The  distinction,  too,  is  inaccurate  from  the  chnical  stand- 
point. As  Sir  William  Osier  says,  there  is  no  benign  endo- 
carditis, for  even  the  most  trivial  acute  infection  may  in- 
augurate changes  of  a  chronic  character,  which  sooner  or  later 
lead  to  death ;  and  an*  infection  which  is  at  first  trivial  in  its 
grade  may  suddenly  assume  a  virulent  character  and  rapidly 
produce  a  fatal  issue.  The  malignant  cases,  too,  may  change 
their  character,  and  the  fire  which  blazed  brightly  at  first  may 
ultimately  burn  itself  out. 

The  Lesions. — In  the  majority  of  cases  acute  endocarditis 
involves  the  valves  of  the  heart  alone,  and  does  not  affect  the 
endothelial  lining  of  the  auricles  and  ventricles.  In  an  early 
case  the  characteristic  festoons  of  little  translucent  white  or 
yellow  beads  are  visible  running  round  the  cusps,  a  little  dis- 
tance from  the  free  margins,  at  the  points  where  the  contact  is 
most  intimate  when  the  valves  are  shut  (Fig.  127).  The  surface 
which  is  exposed  to  the  blood-stream,  the  ventricular  aspect 
of  the  arterial  valves,  and  the  auricular  aspect  of  the  auriculo- 
ventricular  valves  is  alone  implicated.     Microscopic  examina- 

220 


ACUTE  ENDOCARDITIS 


221 


tion  shows  that  the  vegetations  are  mainly  composed  of 
fibrin,  with  a  few  cells  scattered  throughout  the  mass,  and  a 
larger  number  along  the  free  margins.  At  the  base  the  connec- 
tive tissue  of  the  valve  is  hypergemic  and  proliferating,  and  a 


Fig.    127. — Actjte  Veektjcose  Endocarditis,   following  a  Rheumatic   (or 
GoNOCoccic)  Arthritis  (W.  I.  Museum). 


cellular  infiltration  may  be  found.  Micro-organisms  may  be 
detected  with  suitable  staining,  and  are  as  a  rule  most  numerous 
in  the  superficial  layers,  though  they  are  sometimes  seen  in 
the  deeper  layers  and  in  the  valve  itself. 

The  infection  of  the  valve  is  presumably  derived  from  the 


222  DISEASES  OF  THE  HEART 

blood-stream  in,  at  any  rate,  aortic  endocarditis ;  for  there  are 
no  bloodvessels  in  the  normal  aortic  valve,  and  the  bacteria 
gain  access  to  the  tissues  through  some  abrasion  of  the  protec- 
tive endothelium  produced  by  the  toxaemia  and  the  mechanical 
stress  imposed  upon  the  parts.  In  mitral  endocarditis,  how- 
ever, as  vessels  are  present  in  the  valve,  the  deeper  structures 
may  be  first  affected  by  a  bacterial  embolus,  and  the  fibrinous 
exudate  forms  when  the  inflammation  reaches  the  surface,  and 
the  protective  endothelium  is,  in  consequence,  shed.  In  a  case 
of  septicaemia  which  was  shown  to  me  by  Kennedy,  the  infection 
arose  in  an  unusual  way.  An  abscess  had  formed  in  the  inter- 
ventricular septum,  and  reached  the  interior  of  the  right 
ventricle  immediately  beneath  the  septal  cusp  of  the  tricuspid 
valve.  The  latter  became  involved  by  direct  infection,  and 
a  perforation  measuring  nearly  1  cm.  in  diameter  ensued 
in  the  centre  of  the  cusp.  The  free  margin  was  not  affected. 
Acute  endocarditis  is  most  common  on  the  aortic  and  mitral 
valves,  which  are  exposed  to  the  highest  blood-pressure,  and 
bathed  in  the  most  thoroughly  oxygenated  blood. 

In  some  cases  no  bacteria  are  found  on  microscopic  examina- 
tion, and  the  reaction  in  the  valve  is  minimal.  This  is  the 
general  rule  in  the  endocarditis  of  acute  rheumatism,  but 
although  the  lesion  might  follow  a  toxic  and  traumatic 
damage  to  the  valve,  the  general  evidence  in  favour  of  an 
infective  origin  of  acute  rheumatism  is  so  strong  that  one  is 
forced  to  the  conclusion  that  the  cardiac  condition  is  due  to  a 
similar  but  minimal  infection  of  the  valve.  In  the  majority  of 
cases  of  this  type  the  inflammation  in  time  subsides.  The 
vegetations  are  penetrated  by  new-formed  connective  tissue, 
and  the  surrounding  endothelium  grows  over  the  denuded 
surface,  leaving  a  thickened  scar  of  greater  or  of  less  extent. 

In  the  malignant  type  of  case  the  ultimate  result  is  very 
different,  the  bacterial  infection  is  not  overcome,  and  the  infec- 
tion spreads.  In  some  cases  the  vegetations  are  large  and 
luxuriant,  measuring  many  millimetres  in  length  (Fig.  128), 
and  interfering  by  their  mere  bulk  with  the  proper  action  of 
the  valves.  In  others  the  process  is  destructive,  gross  necrotic 
and  ulcerative  processes  ensue,  and  the  cusps  may  be  per- 
forated (Fig.  129),  or  their  attachments  may  be  severed,  and 


ACUTE  ENDOCARDITIS 


223 


their  function  may  be  almost  wholly  abolished.  The  inflam- 
mation, too,  in  some  cases,  spreads  from  the  valves  to  the 
adjacent  parts.  The  spread  is  often  direct,  and  takes  place  in 
any  direction.  If  the  aortic  valve  is  involved,  the  aorta  may 
be  affected,  and  an  acute  infective  aortitis  results,  with  some- 
times  aneurismal  dilatation    (Figs.    129,    130);   or  the  inter- 


-Pneitmococcic  Endocarditis  of  Aoetic  Valve  spreadikg  on  to 

THE  illTPvAL  CirSPS   (W.    I.  MuSETUl). 


Fig.  128.- 
Embolic  gangrene  of  the  foot  ensued  ten  days  after  the  onset  of  the  pneumonia 


ventricular  septum  may  be  infected  (mural  endocarditis),  and 
the  ulceration  may  spread  deeply  into  the  tissues,  and  even 
open  up  communication  with  the  right  side  of  the  heart.  When 
the  mitral  valve  is  implicated,  either  auricle  or  ventricle  may 
be  invaded.  The  most  common  spread  is  upwards  on  to  the 
auricular  wall  opposite  to  the  foramen  ovale   (contra-fossal 


224 


DISEASES  OF  THE  HEART 


wall)  (Fig.  131),  and  downwards  on  to  the  chordae  tendinese 
(which  may  be  ruptured  in  the  process),  sometimes  invading 
even  the  tips  of  the  musculi  papillares. 

In  other  cases  the  infected  area  is  situated  a  little  distance 


Fig.  129. — Malignant  Endocarditis  of  Aortic  V.-vlves,  with  Aneurisms  and 
Perforations  of  the  Cusps;  Infective  Aortitis;  and  Aneurism  of 
Aorta  rupturing  into  Pericardial  Sac  (R.  I.  Museum). 


from  the  valve,  by  an  infected  "  tag  "  waving  to  and  fro  in 
the  blood-stream,  and  hitting  and  infecting  the  ventricular, 
auricular,  or    aortic  walls.     Or  a    fragment  of  a  vegetation 


ACUTE  ENDOCARDITIS  225 

may  be  broken  off,  enter  the  coronary  artery,  and  produce  an 
embolic  abscess  anywhere  in  the  heart. 

The  infective  character  of  mahgnant  cases  is  always  well 
marked,  and  large  collections  of  bacteria  may  be  seen  on  the  sur- 
face of  the  vegetations,  or  more  deeply  situated  in  the  valve  itself. 


Fig.  130. — Pnetjmococcic  Endocaeditis  of  the  Aortic  Valve 
(W.  I.  Museum). 

One  cusp  is  partly  severed  from  its  attachments.  An  aneurism,  the  size  of  a 
walnut,  sprang  from  the  aorta  immediately  above  the  valve,  and  projected 
into  the  right  auricle. 

In  the  intermediate  cases  the  lesions  are  less  extreme  and 
more  chronic  in  their  character.  The  general  evidences  of 
septicsemia  are  absent  or  trifling,  but  a  progressive  valvular 
lesion  can  be  detected  on  physical  examination.  In  the  valves 
themselves  progressive  and  reparative  changes  may  be  seen 

15 


226 


DISEASES  OF  THE  HEART 


side  by  side,  but  the  valvular  defect  is  always  severe,  and  the 
patient  often  dies  from  the  mechanical  fault  even  when  healing 
has  taken  place. 

It  seems  probable  that  in  the  mildest  cases  a  complete  re- 
covery may  occur,  but  pathological  data  are  necessarily  absent ; 


Tig.  131. — Stkeptococcic  Endocarditis  of  Mitral  Valve  speeadestg  on  to 
THE  Left  Auricular  Wall  (W.  I.  Museum). 

The  chordae  tendinese  are  also  involved. 


and  in  the  majority  of  cases,  though  the  infection  is  overcome, 
a  scar  is  left  behind.  The  cardiac  valves  have,  however,  no 
rest,  either  by  day  or  by  night,  and  chronic  fibrous  changes 
ensue,  the  cusps  becoming  thickened  and  shrunken  and  often 
adherent  to  each  other,  and  the  valvular  defect  gradually  but 
steadily  increases  in  degree.     In  time,  after  perhaps   many 


ACUTE  ENDOCARDITIS  227 

years,  it  becomes  extreme,  and  the  cardiac  "pump  "  fails  to 
accomplish  its  necessary  work. 

In  acute  endocarditis  the  cardiac  muscle  is  invariably 
damaged  to  a  greater  or  a  less  degree.  The  gross  infective 
and  ulcerative  lesions  which  occasionally  occur  in  mahgnant 
cases  have,  of  course,  for  long  attracted  notice,  but  the 
microscopic  lesions  have  failed  to  receive  their  due  share  of 
attention,  though  myocarditis  is  an  almost  constant  accom- 
paniment of  acute  endocarditis  (c/.  p.  150).  The  lesions  are 
usually  most  extreme  in  the  vicinity  of  the  base  of  the  affected 
valves,  but  they  are  often  disseminated  widely  through  the 
muscle.  Their  degree  does  not  necessarily  correspond  with 
that  of  the  valvular  inflammation,  and  they  may  be  well 
marked  in  cases  where  the  valvulitis  is  but  trivial.  In  some 
cases  clinical  evidence  of  an  acute  myocarditis  is  available, 
for  the  a.v.  node  and  bundle  are  in  close  proximity  to  the 
mitral,  aortic,  and  tricuspid  valves,  and  may  be  involved  in 
the  inflammation;  and  heart-block,  extra-systoles,  or  nodal 
rhythm  may,  in  consequence,  occur. 

Pericarditis  is  a  frequent  comphcation.  The  flow  of  blood 
and  lymph  takes  place  towards  the  pericardium,  and  its  in- 
fection is  of  common  occurrence,  and  necessarily  adds  greatly 
to  the  gravity  of  the  case. 

The  Causes  of  "Acute  Endocarditis.  —  Acute  Simple  Endo- 
carditis occurs  most  frequently  in  childhood  and  in  adoles- 
cence, though  it  may  be  found  at  any  period  of  life ;  but  accu- 
rate statistics  are  not  available,  for  it  rarely  causes  death 
during  the  acute  stage,  and  post-mortem  data  are,  in  conse- 
quence, awanting.  This  predominance  is  chiefly  due  to  its 
close  connection  with  acute  rheumatism — a  connection  which 
has  been  amply  proved  by  clinical  observation.  In  a  series  of 
1,750  cases  collected  from  the  literature,  933  patients  suffered 
from  endocarditis  ;  and  its  incidence  is  twice  as  great  in  persons 
under  twenty  years  of  age  as  it  is  in  older  persons.  In  children 
under  ten  endocarditis  and  acute  rheumatism  are  almost 
always  conjoined,  and  Norman  Moore  aptly  named  the  disease 
cardiac  fever.  Endocarditis  is  said  to  occur  most  frequently 
in  the  first  attack  of  rheumatism,  and  within  the  first  fortnight 


228  DISEASES  OF  THE  HEART 

of  the  fever;  and  its  incidence  is  not  directly  related  to  the 
severity  of  the  arthritis,  as  it  is  of  common  occurrence  in  cases 
where  the  arthritis  is  trifling  or  subacute,  but  may  be  absent 
though  the  arthritis  is  severe  and  prolonged.  A  recent 
"  claim  "  in  my  insurance  office  illustrates  the  point.  The 
man  died  at  the  age  of  fifty-eight  from  mitral  stenosis.  He 
had  had  muscular  rheumatism  in  1874,  and  rheumatic  pains 
in  his  joints — "  not  rheumatic  fever  " — for  two  or  three  months 
in  1884. 

The  mitral  valve  is  most  frequently  affected,  and  the  valves 
of  the  right  heart  are  but  seldom  involved. 

Endocarditis  is  frequently  associated  with  chorea,  and  was 
present  in  154  cases  of  a  series  of  171  examined  post-mortem. 
Valvular  lesions  are  extremely  common  in  choreic  patients,  and 
were  present  in  262  out  of  829  patients  who  were  examined  during 
or  after  the  illness.  The  endocarditis  is  usually  of  the  simple 
type,  and  though  so  often  present  in  fatal  cases,  is  rarely  the 
immediate  cause  of  death. 

Among  the  exanthemata  endocarditis  is  comparatively  rare, 
but  here  again  post-mortem  data  are  misleading,  as  in  some 
diseases  endocarditis  is  apt  to  be  of  the  malignant  type, 
and  an  active  factor  in  producing  death;  and  its  relative  im- 
portance is,  in  consequence,  over-estimated.  In  pneumonia, 
for  example,  it  was  found  post-mortem  in  16  out  of  100  cases 
(Osier),  but  its  clinical  incidence  is  shght  (0-44  per  cent.,  Musser 
and  Norris).  In  scarlatina  it  only  occurred  in  0-65  per  cent. 
(McCollum).  Macrae  reported  its  occurrence  in  6  of  1,500 
cases  of  enteric  fever,  and  Horton-Smith  in  4  of  290  cases  ex- 
amined post-mortem  ;  and  Councilman  in  1  out  of  54  (post- 
mortem) cases  of  smallpox.  Horder  has  recorded  its  occurrence 
in  influenza. 

The  causes  of  acute  endocarditis,  with  the  exception  of  acute 
rheumatism  and  chorea,  are  thus  unknown,  and  it  has  been 
suggested  that  the  other  "  rheumatic  "  manifestations,  acute 
tonsillitis,  erythema  nodosum,  etc.,  may  be  responsible.  The 
suggestion  is  extremely  plausible,  for  the  tonsils  are  recognized 
to  be  the  harbourers  of  many  micro-organisms,  and  they  not 
infrequently  show  on  section  macroscopic  evidence  of  gross 
infection  of  the  crypts  which  was  not  evident  on  examination 


ACUTE  ENDOCARDITIS  229 

of  the  surface;  and  the  probabihty  of  a  blood-infection  is 
increased  if  the  middle  ears  and  the  naso-pharynx  are,  as  is  so 
frequently  the  case,  also  inflamed. 

It  must  be  remembered,  however,  that  the  portal  of  entry  in 
malignant  cases  is  not  always  evident,  even  on  post-mortem 
examination,  and  in  these  cases  must  have  been  trivial  and  of 
short  duration ;  and  a  similar  trivial  sepsis  may  be  responsible 
for  some  of  the  simple  cases. 

In  the  malignant  cases  the  valves  which  are  involved  have 
been  as  a  rule  already  damaged,  and  are,  in  consequence, 
places  of  lessened  resistance,  so  that  the  disease  affects  older 
people  than  in  the  case  of  the  simple  form.  In  Kanthack  and 
Tickell's  series  of  84  cases,  only  25  were  under  twenty  years 
of  age,  and  in  Border's  series  of  150,  only  45.  In  my  series 
the  proportion  is  larger — 14  out  of  30  cases.  The  valves 
had  been  previously  damaged  in  64  per  cent,  of  Kanthack's 
and  80  per  cent,  of  Kelynack's  series;  in  108  cases  out  of 
118  of  Border's  series;  and  in  24  of  my  series  of  30.  Malig- 
nant cases  are,  however,  not  uncommon  in  the  second  decade, 
perhaps  in  consequence  of  the  special  incidence  of  acute  rheu- 
matism at  this  period. 

The  association  with  acute  rheumatism  is  again  extremely 
close,  but  the  nature  of  the  connection  is  not  clear.  Rheuma- 
tism may  act  merely  as  a  predisposing  cause  by  damaging  the 
valves  and  so  allowing  a  subsequent  bacterial  infection  from 
a  minimal  dose ;  or  by  producing  a  mahgnant  form  of  endo- 
carditis. Poynton  has  emphasized  the  latter  view,  and  has 
isolated  the  micrococcus  in  blood-culture  on  several  occasions. 
In  one  of  my  cases  Kennedy  isolated  a  similar  organism  both 
during  life  and  after  death.  But  Horder  considers  that  mahg- 
nant rheumatic  cases  are  due  to  a  superadded  infection.  In 
the  typical  endocarditis  of  acute  rheumatism,  at  any  rate,  blood- 
cultures  are  ahnost  always  sterile. 

The  association  with  other  infections  is  by  no  means  close. 
The  majority  of  these  patients  have,  of  course,  suffered  from 
some  of  the  exanthemata  in  early  life,  or  from  some  infection, 
but  in  a  few  cases  no  antecedent  illness  has  been  known.  In 
others,  however,  many  infections  have  been  present,  and  one 
of  my  patients,  a  man  of  twenty-four  year?,  had  suffered  from 


230  DISEASES  OF  THE  HEART 

growing-pains,  enteric  fever,  diplitlieria,  pneumonia,  and  gonor- 
rhoea ;  lie  was,  too,  liable  to  boils,  and  his  mouth  was  extremely- 
septic,  the  gums  being  swollen  and  bleeding  on  shght  provoca- 
tion. A  similar  state  of  extreme  oral  sepsis  was  present  in 
another  patient,  while  a  third  had  an  offensive  rhinitis,  and  a 
fourth  a  chronic  otorrhoea.  In  two  of  my  cases  the  symptoms 
developed  during  lactation,  though  there  was  no  obvious  source 
of  sepsis  about  the  uterus  or  breasts. 

In  another  case  the  symptoms  succeeded  the  birth  of  the 
patient's  second  child.  She  had  frequent  rigors,  with  profuse 
perspiration,  which  recurred  every  two  or  three  days.  The 
lochia  persisted  for  six  weeks,  and  only  finally  cleared  after 
"  a  copious  discharge  "  had  continued  for  a  few  days. 

In  another  the  sj^mptoms  succeeded  a  "  cross-birth  "  twelve 
weeks  before  admission  to  hospital.  Rigors  occurred  on  the 
third  or  fourth  day  afterwards,  and  were  frequently  repeated, 
and  she  felt  pain  in  her  left  side  when  she  coughed.  Post- 
mortem examination  revealed  the  association.  The  uterus  was 
small  and  involuted,  but  the  endometrium  showed  evidence  of 
recent  ulceration,  and  many  thrombosed  veins  were  present 
in  the  muscular  wall.  The  right  ovarian  vein  contained  a  long 
thrombus,  and  there  were  clots  in  the  iliac  veins  and  the  lower 
3  inches  of  the  inferior  vena  cava ;  these  did  not,  however,  com- 
pletely block  the  lumen.  There. was  a  large,  dense,  mobile 
thrombus,  the  size  of  a  marble,  in  the  right  auricle,  and  a 
smaller  one  attached  to  the  wall.  The  mitral  valve  was  covered 
with  fairly  large,  soft,  fibrinous  vegetations,  and  the  tricuspid 
valve  was  also  affected,  but  in  lesser  degree.  Septic  abscesses 
were  present  in  the  spleen  and  in  the  lungs,  and  a  large  necrosis 
of  the  visceral  pleura  had  produced  a  pneumothorax,  which  was 
the  immediate  cause  of  death.  Blood-cultures  during  life  were 
sterile. 

Hearts  with  congenital  defects  are  not  infrequently  affected. 

The  valves  on  the  left  side  of  the  heart  are  those  which  are 
most  frequently  involved,  but  the  great  predominance  of  mitral 
disease  in  simple  endocarditis  is  not  approached,  though  this 
valve  is  more  often  infected  than  the  others.  Two  or  more 
valves  are  involved  in  nearly  hah  the  cases,  and  a  mural 
infection  occurs  in  about  a  quarter. 


ACUTE  ENDOCARDITIS 


231 


Recent  improvements  in  blood-culture  have  led  to  the  isola- 
tion, during  life,  of  the  causal  micro-organism  in  a  large  number 
of  cases,  but  Horder's  positive  results  (29  out  of  32)  are  more 
numerous  than  are  usually  obtained.  The  micro-organism  is 
generally  isolated  in  acute  cases,  and  less  frequentty  in  the 
chronic  types — at  any  rate,  until  shorth^  before  death.  In  my 
series  positive  results  were  obtained  in  3  out  of  11  cases;  in  Sir 
William  Osier's,  in  3  out  of  6.  The  most  common  organism  is 
a  streptococcus  of  low  virulence,  which  is  closely  "allied  to 
the  saprophytic  streptococci  of  the  ahmentary  tract  "  (Horder). 

The  characters  of  the  vegetations  are  not  specific,  but  in  a 
general  way  the  pneumococcic  and  gonococcic  vegetations  are 
numerous  and  small,  while  staphylococci  produce  a  spreading 
ulceration. 

Acute  Soiple  Exdocakditis. 


Cases  of  Acute 
Rheumatism. 

Cases  of 
Endocarditis. 

Sibson 

Macrae 

Churcli 

Moore 

Latham 

325 
300 

889 
100 
136 

161 
105 

494 
99 

74 

1,750 

933 

First  Attacks  (Church) — 

16  cases  under  10  years:  endocarditis  in  12 — 75  per  cent, 

109      ,,     between  10  and  20:         „  60—55      „ 

75      „     between  20  and  30:         ,,  38—50       „ 

36      ,,     between  30  and  40:         „  13—36      „ 

8      „     over  40:  „  1—12      „ 

Endocarditis  was  present  in  149  out  of  150  fatal  cases  of  acute 
rheumatism  under  the  age  of  twelve  (Poynton).  In  Macrae's 
series  it  was  present  in  45  per  cent,  of  cases  under  twenty  years, 
but  only  in  20  per  cent,  of  cases  over  twenty  years. 

In  Sibson's  series  murmurs  made  their  appearance  in  25  per 
cent,  of  cases  within  the  first  week,  and  in  66  per  cent,  within 
the  first  two  weeks  of  the  disease. 

In  Macrae's  series  the  mitral  valve  alone  was  affected  in 
77  per  cent.,  the  aortic  valve  alone  in  5  per  cent.,  and  both  in 


232 


DISEASES  OF  THE  HEART 


18  per  cent.  At  St.  Thomas's  Hospital  the  corresponding 
figures  were:  Mitral  valve  alone,  85  per  cent.;  aortic  valve 
alone,  3  per  cent. ;  and  both  in  12  per  cent. 


Malignant  Acute  Endocarditis. 


Horder, 

Personal, 

Age. 

150. 

30. 

1  to  10         

7 

1 

10  „  20        

38 

13 

20  „  30        

39 

8 

30  „  40        

31 

2 

40  „  50        

23 

3 

50  „  60        

8 

3 

60  and  over 

4 

— 

Sex: 

Male          

79 

17 

Female 

71 

13 

Osier, 

Horder, 

Personal, 

Total, 

209  Cases. 

lis  Cases. 

•29  Cases. 

356. 

Mitral          

77 

38 

8 

123 

Aortic 

53 

22 

2 

77 

Mitral  and  aortic    . . 

41 

63 

13 

117 

Tricuspid  and  others 

19 

14 

5 

38 

Pulmonary  and  others 

15 

7 

1 

23 

Mural  infection 

33 

51 

4 

88 

Valves  of  right  heart  alone 

9 

— 

— 

9 

Congenital  defects  in  heart 

— 

8 

1 

9 

Previous  Infections. 

Personal, 
28  Cases. 

Horder, 
loO  Cases. 

Acute  rheumatism 

13 

}  72 

Chorea 

4 

Tonsillitis    . . 

3 



Pneumonia 

6 

1 

Enteric  fever 

1 

4 

Diphtheria  . . 

1 

— 

Scarlet  fever 

— 

10 

Influenza     . . 

— 

2 

Dysentery   . . 

— 

1 

Gonorrhoea 

— 

7 

Extreme  oral  sepsis 

2 



Atrophic  rhinitis    . . 

1 

— 

Otorrhcea     . . 

1 

— 

Lactation    , . 

2 



Fistula         

I 

ACUTE  ENDOCARDITIS 


233 


The  records  being  derived  from  hospital  patients  are  almost 
certainly  defective  in  many  respects. 


Organisms  isolated  during  Life. 

Horder. 

Personal. 

Streptococcus 

Bacillus  infliienzcE 

Pneumococcus 

Gonococcus 

Staphylococcus  alhus 

Doubtful 

26 
5 
5 
2 
1 
1 

1 
1 
1 

E.  Libman  has  recently  described  a  group  of  cases  of  sub- 
acute endocarditis  and  has  isolated  a  streptococcus  in  71  out 
of  75  cases.  He  names  the  organism  Streptococcus  mitis.  It 
is  probably  the  same  as  the  >S',  viridans  and  the  S.  salivarius 
of  other  writers. 

In  surgical  cases  the  most  common  organisms  are  the 
Staphylococcus  aureus  and  the  Streptococcus  pyogenes. 


EEFERENCES. 

T.  J.  Hoeder:  Quart.  Joum.  of  Med.,  1908-09,  vol.  ii. 
SmW.  Oslek: 

Ibid.,  p.  133. 

Osier's  System,  1908,  vol.  iv.,  p.  219. 
E.  Libman: 

Amer.  Journ.  Med.  Sci.,  1912,  vol.  cxliv.,  p.  313. 

Ibid.,  1913,  vol.  cxlvi.,  p.  625. 

Trans.  Intemat.  Med.  Congress,  London,  1913. 


p.  289. 


CHAPTER  XIX 
ACUTE  ENDOCARDITIS— Co7^iwM 

The  Symptoms. 

In  the  majority  of  cases  of  simple  acute  endocarcTitis  occur- 
ring in  the  course  of  rheumatic  fever,  the  patient  makes  no 
complaint  of  any  cardiac  symptoms,  and  a  valvular  lesion 
is  discovered  on  routine  examination  of  the  heart.  Occasion- 
ally palpitation  or  discomfort  or  even  slight  pain  in  the  cardiac 
region  may  be  experienced,  but  these  are  rare  in  the  absence 
of  pericarditis.  There  is  seldom  any  dyspnoea,  and  the  chief 
discomforts  are  the  pain  of  the  arthritis  or  the  profuse  sweating. 

The  onset  of  endocarditis  is,  however,  as  a  rule  associated 
"\\ith  definite  evidence  of  cardiac  embarrassment.  The  most 
constant  signs  are  found  in  the  pulse,  which  may  be  more  fre- 
quent than  the  degree  of  fever  would  suggest,  or  infrequent,  or 
irregular;  and  the  abnormahty  may  persist,  even  unchanged, 
though  the  fever  and  the  arthritis  subside,  and  convalescence 
is  apparently  attained.  As  an  isolated  symptom,  an  abnormal 
rate  or  rhythm  is  extremely  suggestive,  and  may  be  present  at 
a  time  when  valvular  murmurs  are  absent. 

A  girl  of  fifteen  was  admitted  to  my  wards  suffering  from 
subacute  rheumatism  which  had  lasted  for  some  six  weeks. 
Within  a  week  the  arthritis  had  subsided,  and  the  joints  were 
mobile  and  painless.  The  heart  seemed  normal  on  examina- 
tion, but  the  pulse-rate  continued  to  be  high  (90  to  100)  after 
the  fever  had  disappeared.  A  month  later  a  very  soft  blowing 
murmur  made  its  appearance  for  the  first  time  at  the  apex, 
and  the  second  pulmonic  sound  became  accentuated.  Four 
months  afterwards  the  recognition  of  a  typical  presystohc 
murmur  placed  the  diagnosis  of  organic  valvular  disease  beyond 
doubt. 

234 


ACUTE  ENDOCARDITIS 


235 


In  manv  of  these  cases  the  recurrence  of  rheumatic  symp- 
-toms  (arthritis,  tonsilhtis,  chorea,  nodules)  emphasizes  the  fact 
that  the  infection  is 
not  completely 
•eradicated,  but  re- 
currence is  extremely 
rare  if  the  pulse-rate 
has  returned  to  nor- 
mal figures .  One 
iaUacy,  however, 
must  be  remembered . 
The  pulse-rate  during 
the  administration  of 
-saUcylates  is  often 
within  normal  hmits, 
but  rises  on  its  with- 
•drawal,  so  that  the 
pulse  should  be  ob- 
served for  at  least  a 
week  after  the  ad- 
ministration of  sali- 
cylates has  been 
■ceased  before  any 
conclusion  is  reached 
<Fig.  132). 

The  pulse  in  endo- 
carditis is  not  infre- 
•q  u  e  n  1 1  y  itregular . 
This  may  be  due  to 
partial  heart-block, 
which  I  have  now 
observed  in  six  cases. 
In  one  the  defect  per- 
sisted for  nearly  four 
weeks ;  in  another  it 
disappeared  after  six 
days,  but  recurred  three  days  later,  again  lasting  for  six  days ; 
in  a  third  it  was  present  for  several  weeks  before  death;  in 
the  others  it  was  transient,  and  only  present  for  a  few  days. 


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Fig.  132.— Chakt  of  J.  McK.,  Aged  7.    Acute 
Rheumatism;  JIiteal  Endocaeditis. 

Note  rise  of  pulse-rate  on  cessation  of  salicylate  ( X  ). 
The  temperature  had  been  normal  for  thirteen 
days. 


236  DISEASES  OF  THE  HEART 

Heart-block  in  varying  degree  has  been  reported  in  gonococcic 
and  streptococcic  infections,  and  though  it  may  occur  in  the 
infections  apart  from  endocarditis  (diphtheria — Fleming),  the 
two  are  so  commonly  associated  that  their  co-existence  is 
extremely  probable.  An  infrequent  pulse  is  generally  due  to 
full  heart-block. 

Extra-systoles  may  also  occur.  I  have  seen  them  in  seven 
patients,  in  three  of  whom  nodal  rhythm  ultimately  ensued. 
Extra-systoles  are,  of  course,  of  common  occurrence  in  various 
forms  of  cardiac  disease,  as  well  as  in  patients  whose  hearts 
are  apparently  normal,  and  their  appearance  can  only  b& 
taken  as  suggestive  of  an  acute  cardiac  lesion  when  they  recur 
frequently  without  other  signs  of  cardiac  distress. 

Auricular  fibrillation  occurs  occasionally,  but  I  have  only 
seen  it  as  a  terminal  event,  and  it  obtains  in  so  many  dying 
hearts  that  its  significance  is  slight. 

The  persistent  form  of  nodal  rhythm  seems  usually  to  be 
associated  with  acute  endocarditis,  which  was  found  to  be 
present  in  six  of  my  cases  on  post-mortem  examination.  In  a 
seventh  case  the  clinical  course  of  the  illness  suggested  a  similar 
diagnosis,  but  no  post-mortem  examination  was  obtained.  In 
another  case  the  lesions  were  perhaps  chronic. 

"  Cardiac  overaciion  "  is  often  present,  the  vehemence  of  the 
cardiac  pulsations  widely  diffused  over  many  interspaces  being 
associated  with  a  pulse  which  is  small  and  soft  to  a  degree 
which  is  quite  out  of  proportion  to  the  apparent  strength  of  the- 
heart.     Cardiac  overaction,  however,  owns  several  causes. 

It  is  often  present  in  hypertrophied  hearts — in  particular, 
those  associated  with  aortic  regurgitation.  It  is  almost  always 
present  in  paroxj^smal  tachycardia,  and  is  frequently  seen  in 
cases  of  exophthalmic  goitre  when  the  pulse-rate  is  frequent. 

In  paroxysmal  tachycardia  its  origin  is  obvious.  Auricle 
and  ventricle  are  contracting  simultaneously,  and  the  auriculo- 
ventricular  valves  are  consequently  shut,  so  that  the  ventricular 
output  must  be  limited;  while  the  obstacle  opposed  to  the 
auricles,  and  to  the  right  ventricle  in  consequence,  leads  to 
vigorous  though  ineffective  attempts  to  overcome  the  diffi- 
culty. A  similar  state  of  matters  may  also  obtain  in  cases 
where   the  pulse-rate   is    frequent,  though   the   beats  are  of 


ACUTE  ENDOCARDITIS  237 

sinus  origin ;  for  if  the  rate  of  stimulus  production  is  sufficient^ 
rapid,  auricular  systole  will  occur  before  the  preceding  ven- 
tricular systole  has  ended,  and  a  similar  interference  with  the 
onward  flow  of  blood  will,  in  consequence,  ensue. 

The  auscultatory  evidence  of  endocarditis  may  be  definite 
quite  early  in  the  illness,  even  before  the  arthritis  has  subsided 
or  the  associated  fever  gone.  But  a  systolic  murmur,  it  must 
be  remembered,  may  be  of  functional  (myocardial)  origin,  and 
is  extremely  likely  to  accompany  the  anaemia  which  is  so 
rapidly  produced  by  acute  rheumatism.  In  some  cases,  too, 
the  cardiac  sounds  are  pure  at  first,  and  a  murmur  only  develops 
during  convalescence. 

The  early  auscultatory  signs  may  be  very  trivial,  and  a  slight 
blurring  or  roughening  of  the  first  sound,  or  a  short  distant 
and  muffled  sound,  or  a  short  sharp  often  loud  sound,  approxi- 
mating in  character  to  that  of  the  normal  second  sound,  may 
be  the  precursors  of  the  permanent  murmur  of  organic  valvular 
disease.  Murmurs  are  apt  to  be  intermittent  in  the  early 
stages,  and  may  be  distinct  one  day,  and  faint  or  gone  upon 
the  next,  to  recur  in  course  of  time.  I  have  noticed  this  on 
many  occasions,  and  in  some  which  were  examined  'post- 
mortem  the  valves  were  covered  with  very  large  vegetations, 
which  by  their  bulk  were  quite  capable  of  closing  the  aperture. 
In  one  case  where  an  infective  endocarditis  involved  a  pulmonic 
valve  which  was  congenitally  defective,  one  of  the  longest 
and  loudest  diastolic  murmurs  which  I  have  ever  heard  dis- 
appeared altogether  for  several  days,  though  it  returned  before 
death. 

The  occurrence  of  pericarditis  or  the  appearance  of  sub- 
cutaneous nodules  are  additional  evidence  in  favour  of  an  endo- 
carditis being  acute.  Pericarditis  is  almost  invariably  accom- 
panied by  endocarditis,  though  the  degree  of  the  two  is  by  no 
means  proportionate,  and  either  may  be  severe  when  the  other 
is  slight.  Subcutaneous  nodules  are  generally  considered  to 
be  indicative  of  gross  cardiac  inflammation — endocardial,  peri- 
cardial, or  myocardial  —  an  opinion  with  which  my  own 
experience  agrees,  but  the  endocarditis  is  not  necessarily 
severe. 

Subcutaneous  nodules  are  usually  small  (pin-head  to  a  large 


238  DISEASES  OF  THE  HEART 

pea),  fairh-  firm  in  consistence,  painless  and  not  tender,  and 
freely  movable  beneath  the  skin  and  upon  the  subjacent 
tissues.  Tenderness  may  be  present  if  they  are  mechanically 
irritated.  They  are  most  common  about  the  back  of  the  hand, 
the  elbow,  the  knee,  the  scapula,  and  the  occiput,  occurring  in 
relation  to  the  fibrous  planes,  the  hgaments,  and  the  tendon 
sheaths ;  but  I  have  seen  them  on  almost  every  part  of  the 
body  save  the  face.  Comparable  lesions,  too,  occur  in  the 
muscles.  In  one  case  the  patient  frequently  complained  of 
pain  in  different  muscles,  which  were  tender  to  the  touch. 
As  a  rule,  nothing  abnormal  could  be  felt,  but  sometimes  an 
indefinite  induration  was  apparent,  which  disappeared  in  a 
day  or  two.  In  another  patient  the  lesions  were  ver\'  large, 
and  one  reached  the  size  of  a  hen's  egg,  the  surrounding  tissues 
becoming  brawny  and  infiltrated.  The  left  sterno-mastoid 
was  affected  at  one  time,  and  the  swelling  which  commenced 
at  its  uppey  extremity  gradually  spread  downwards  to  the 
sternal  insertion.  Suppuration  did  not  result,  but  the  muscle 
remained  indurated  and  hard  for  a  week  after  the  swelling  had 
subsided. 

In  the  majority  of  cases  the  nodules  are  discovered  acci- 
dentally, and  a  routine  examination  reveals  several.  In  some 
patients  fifty  or  more  may  be  present  at  one  time.  Thej^  last 
for  a  variable  period — a  da}^  or  two  or  several  weeks — irrespec- 
tive of  their  size,  and  resolution  is  complete.  A  migrator}- 
circinate  erythema  is  a  common  accompaniment. 

The  continuance  of  fever  after  the  arthritis  has  subsided,  or 
a  want  of  correspondence  between  its  degree  and  that  of  the 
joint  affection,  have  as  their  most  common  cause  an  endocar- 
ditis. Endocarditis  is  generall}-  present  in  cases  where  the 
arthritis  relapses,  even  if  the  recrudescence  is  shght  and  tem- 
porary; and  in  cases  where  the  other  manifestations  of  the 
rheumatic  poison,  chorea,  tonsiUitis,  erythema,  etc.,  occur 
subsequently,  perhaps,  in  quick  succession. 

The  symptoms  of  the  graver  forms  of  the  disease  are  very 
varied,  as  they  may  be  referable  to  almost  any  organ.  Endo- 
carditis may  be  merely  a  part  of  a  general  pyaemia,  a  meta- 
stasis from  the  original  septic  focus,  and  may  occasion  httle  in 
the  w-ay  of  symptoms,  and  have  little  direct  comiection  with 


ACUTE  ENDOCARDITIS  239 

the  fatal  issue  of  the  case.  A  girl  of  nine,  for  instance,  who 
had  suffered  from  otitis  media,  noticed  that  her  ears  had  again 
begun  to  discharge.  A  few  days  later  a  broncho-pneumonia 
developed,  from  which  she  seemed  to  be  convalescing,  when 
meningeal  symptoms  made  their  appearance  and  rapidly  caused 
death.  At  the  post-mortem  examination  vegetations  were 
found  on  the  aortic,  mitral,  and  pulmonary  valves,  and  seemed 
the  probable  source  of  the  meningeal  infection. 

In  another  group  of  cases  endocarditis  is  merely  a  terminal 
event,  occurring  in  a  patient  who  is  dying  slowly  from  a 
chronic  disease.  In  one  of  my  patients  who  suffered  from  a 
pneumococcic  endocarditis  of  the  aortic  and  mitral  valves  and 
the  left  auricle,  there  was  found  'post-mortem  a  quiescent  tuber- 
cular lesion  at  an  apex,  a  cancerous  ulcer  in  the  stomach, 
granular  kidneys,  and  several  strictures  of  the  urethra  !  In 
another  group  embohc  phenomena  may  be  the  first  indication 
of  the  presence  of  serious  cardiac  mischief.  A  woman  aged 
thirt^'-four,  who  had  suffered  from  several  attacks  of  acute 
rheumatism  during  adolescence,  complained  of  epistaxis  and 
of  throbbing  in  the  head  during  the  later  months  of  her  fourth 
pregnancy.  The  confinement  (triplets)  in  August  was  unevent- 
ful, and  she  made  a  good  convalescence,  though  the  throbbing 
continued.  In  the  second  week  of  October  hemiplegia  sud- 
denly ensued,  from  which  she  died  three  days  later.  Post- 
mortem examination  revealed  an  acute  endocarditis  of  the 
mitral  valve  and  the  left  auricle,  and  a  cerebral  haemorrhage 
which  had  ruptured  into  the  ventricles. 

The  symptoms  are  perhaps  best  illustrated  by  consideration 
of  a  number  of  cases  in  detail. 

In  some  instances  endocarditis  is  subacute  but  persistent, 
and  serious  symptoms  only  ensue  after  many  months.  The 
bacteria  concerned  may  be  of  various  kinds,  and  the  cardiac 
infection  may  seem  trivial  at  first,  even  when  it  is  the  source  of 
the  recurring  symptoms  elsewhere.  This  is  often  the  case  in 
the  "rheumatic  "  group. 

Case  1. — A  well-grown  girl  of  fifteen,  who  had  had  no  serious 
illness,  contracted  an  attack  of  acute  rheumatism  in  December, 
1910,  which  kept  her  in  bed  for  two  months.  In  April,  1911, 
chorea  supervened  and  persisted  for  six  weeks,  and  it  recurred  in 


240  DISEASES  OF  THE  HEART 

June  for  nearly  a  month.  In  November  she  again  suffered  from 
arthritis,  this  time  for  three  weeks,  and  it  returned  in  January 
and  in  April,  1912,  for  a  few  days. 

The  associated  cardiac  phenomena  were  instructive.  On 
her  first  admission  in  April,  1911,  the  heart  was  of  normal  size, 
but  a  systolic  murmur  was  audible  at  the  apex,  running  out 
of  the  first  sound  for  a  considerable  distance  into  the  short 
pause.  The  second  pulmonic  sound  was  accentuated.  No 
change  was  apparent  during  her  second  residence  in  June,  save 
that  the  murmur  was  longer  and  louder.  On  admission  in 
November  the  left  heart  was  distinctly  larger  than  before,  but 
it  resumed  its  former  size  within  a  month,  coincidently  with 
the  subsidence  of  the  arthritis.  The  murmur  was  unchanged, 
but  a  new  diastolic  murmur  of  aortic  distribution  made  its 
appearance  in  the  middle  of  December.  Towards  the  end  of 
that  month  she  complained  of  pain  in  the  upper  part  of  the 
chest  for  a  few  days,  and  this  recurred  in  the  middle  of  Febru- 
ary, 1912,  and  in  the  first  week  of  March.  A  double  murmur 
was  now  audible  over  the  sternum,  and  she  complained  con- 
tinually of  pain  in  the  chest,  though  no  pericardial  friction 
could  be  detected.  But  in  the  middle  of  April  the  tempera- 
ture again  rose,  and  friction  sounds  became  audible  all  over 
the  heart,  and  an  effusion  of  moderate  size  rapidly  developed . 
By  the  end  of  May  the  effusion  had  to  a  large  extent  dis- 
appeared, but  both  hearts  were  large,  and  the  aortic  and  mitral 
murmurs  persisted.  She  made  a  fair  convalescence,  and  in 
the  autumn  was  able  to  do  her  share  of  the  housework.  In 
December  a  pulmonary  infarct  occurred,  and  she  died  in 
February,  1913,  from  cardiac  failure  (c/.  p.  143). 

In  rheumatic  endocarditis  the  arthritic  symptoms  may 
be  trifling,  even  when  the  cardiac  affection  is  severe,  and 
this  is  more  hkely  to  be  the  case  in  childhood  than  in  adult 
life.     The  cardiac  inflammation,  too,  may  run  an  acute  course. 

Case  2. — An  Italian,  aged  eighteen,  was  admitted  into  my 
wards  complaining  of  pains  in  the  joints  and  in  the  chest  and 
of  palpitation  and  general  weakness.  He  had  suffered  from 
acute  rheumatism  three  years  before,  but  had  made  a  good 
recovery,  and  his  present  symptoms  only  began  five  weeks 
before  admission.     He  rapidly  became  pale  and  felt  weak  and 


ACUTE  ENDOCARDITIS  241 

giddy  when  at  work,  so  that  he  was  forced  to  take  to  bed  ten 
days  after  the  onset  of  symptoms . 

On  admission,  he  was  found  to  be  well  developed  and  well 
nourished.  He  looked  extremely  pale  and  complained  of  pain 
in  his  joints  on  movement,  though  the  left  ankle  alone  was 
tender  and  swollen.  There  was  slight  oedema  in  both  feet. 
He  lay  fiat  in  bed,  and  breathed  easity  and  quietty ;  the  lungs 
were  normal.  The  mouth  contained  many  carious  teeth,  and 
the  tongue  was  slightly  furred.  The  liver  was  enlarged  and 
shghtly  tender;  the  stools  were  normal.  The  thj^roid  gland 
was  shghtly  enlarged  and  was  tender  on  palpation.  The 
urine  contained  a  trace  of  albumin.  Eor  two  days  after  ad- 
mission he  seemed  to  improve,  his  discomforts  abating  and 
his  puhe  and  temperature  rumiing  at  normal  rates,  but  on  the 
evening  of  December  5  his  temperature  rose  to  99' 6"^  F.  and  to 
higher  hmits  in  the  days  succeeding,  touching  a  maximum  of 
104*4°  F.  on  December  21,  though  the  morning  remission 
touched  or  approached  the  normal.  Fresh  symptoms,  too, 
began  to  appear,  and  he  complained  at  this  time,  for  a  couple 
of  days,  of  pain  in  his  right  forearm,  which  was  found  to  be 
tender  and  shghtly  swollen.  A  few  days  later  his  left  shoulder- 
joint  Avas  painful  on  movement,  though  nothing  objective 
could  be  discovered.  The  fever  persisted,  and  he  became 
steadily  weaker.  Rales  appeared  at  the  bases  of  the  lungs  in  the 
second  week  of  January,  and  the  oedema  of  the  feet  reappeared. 
Blood  was  found  in  the  urine  on  January  22,  and  became 
considerable  in  amount,  incontinence  of  urine  ensued,  and  he 
became  delirious  at  night.  He  died  from  increasing  cardiac 
weakness  on  January  31. 

The  special  interest  of  the  case  is  concerned  with  the  heart, 
Avhich,  on  admission,  was  enlarged  on  both  sides. 

Double  murmurs  were  audible  all  over  the  sternum  as  well 
as  a  systohc  murmur  at  the  apex,  which  was  thought  to  indi- 
cate mitral  reflux.  The  pulse  was  large  and  notably  shotty. 
For  the  first  few  days  of  his  residence  its  rate  varied  from 
80  to  89,  but  it  then  increased  to  90-110,  and  touched  128 
on  the  evening  of  December  31,  when  the  fever  was  high.  It 
was  habitually  regular  and  large,  but  from  December  25  to  27 

was  noticed  to  be  much  less  in  volume  than  before,  though  no 

16 


242  DISEASES  OF  THE  HEART 

other  abnormality  was  detected.  After  January  14  it  became 
more  frequent  and  averaged  about  110,  and  after  January  21, 
1912,  numbered  about  120  beats  per  minute,  touching  a  maxi- 
mum of  140  on  January  28.  It  was  habitually  regular  save 
on  January  24,  when  it  was  noticed  to  be  grossly  irregular 
for  a  couple  of  hours,  and  this  was  accompanied  by  grave 
symptoms  of  cardiac  exhaustion,  from  which,  however,  he 
rallied  next  morning;  and  after  January  29,  until  death  on 
January  31. 

The  highest  leucocyte  count,  on  January  24,  numbered 
13,000.  A  blood-culture  on  January  17  showed  the  presence 
of  diplococci  (?  Micrococcus  rheumaticus) . 

Polygraph  records  were  taken  regularl}^  and  were  easily 
secured  until  January    16,   but   thereafter  were  difficult   to 


Fig.  133. — Nodal  Rhythm  (Case  2.). 

obtain  on  account  of  the  respiratory  distress  and  overaction 
of  the  sterno-mastoid  muscle.  In  the  early  tracings  the  a-c 
interval  averaged,  or  even  exceeded,  0*20  second,  and  a  partial 
block  was  carefully  watched  for;  but  the  interval  tended  to 
decrease  rather  than  to  increase,  and  on  January  8  was  dis- 
tinctly less  than  0*20  second,  and  it  barely  exceeded  0*10  second 
on  January  16.  On  January  19  the  A-V  interval  in  the  apex 
tracing  only  ohghtly  exceeded  0"05  second,  and  on  January  25, 
following  the  period  of  irregularity  on  the  preceding  evening, 
the  a-c  interval  in  the  jugular  curve  was  definitely  shown  to 
be  habitually  less  than  O'lO  second.  Tracings  thereafter  were 
undecipherable  (c/.  Nodal  Rhythm,  Chapter  X.). 

On  post-mortem  examination,  the  heart  was  found  to  be 
greatly  enlarged.  The  pericardial  sac  contained  a  small 
amount  of  fibrinous  exudation,  and  the  parietal  pericardium 
presented  several  patches  of  fibrosis  over  both  auricles  and 
ventricles.     The   aortic   cusps    were   covered   with   luxuriant 


ACUTE  ENDOCARDITIS  243 

vegetations,  which  spread  downwards  for  a  short  distance  on 
to  the  adjacent  ventricular  wall.  The  mitral  valve  was  simi- 
larly affected,  and  the  vegetations  involved  some  of  the  chords 
tendineae  and  the  left  auricular  wall.  Both  valves  showed 
evidence  of  old-standing  fibrosis.  The  spleen  showed  many 
infarctions,  and  an  acute  parenchymatous  nephritis  was  super- 
added to  a  chronic  interstitial  inflammation. 

The  cardiac  muscle  was  seriously  damaged.  Extensive 
cellular  infiltrations  were  found  in  both  ventricle  and  auricle, 
in  greatest  degree  around  the  bases  of  the  valves,  and  diffuse 
and  focal  collections  were  present  farther  away,  involving  to 
a  notable  degree  the  a.v.  node,  but  barely  touching  the  a.v. 
bundle.  The  s.a.  node  showed  no  evidence  of  recent  in- 
flammation, but  around  its  artery  there  was  considerable 
fibrosis,  which  spread  into  the  adjacent  nodal  tissue.  The 
epicardium  was  somewhat  thickened,  and  strands  of  fibrinous 
tissue  spread  from  it  into  the  node,  and  infiltrated  between 
the  nerve  fibres  and  the  ganglion  cells . 

The  diagnosis  in  this  case  was  not  difficult,  the  continuance 
of  the  fever  being  associated  with  a  visceral  lesion  in  the  heart 
alone.  The  progressive  cardiac  weakness  and  the  occurrence 
of  nodal  rhythm  pointed  in  the  same  direction. 

In  other  cases,  however,  the  cardiac  symptoms  may  be  shght 
and  the  duration  of  a  valvular  flaw  unknown,  so  that  its  rela- 
tion to  septicsemic  symptoms  is  difficult  to  establish.  The 
occurrence  of  embolic  phenomena  is,  however,  extremely  sug- 
gestive of  acute  endocarditis,  and  in  the  following  case  led  to  a 
correct  diagnosis. 

Case  3. — 'The  patient,  a  man  aged  twenty-six  years,  was 
admitted  into  hospital  on  June  5,  1909,  complaining  of  weak- 
ness and  of  breathlessness  on  exertion  of  some  months' 
duration. 

The  patient's  health  had  been  good,  save  for  occasional 
"growing-pains,"  an  attack  of  tonsillitis  in  boyhood,  and 
gonorrhoea  in  the  early  part  of  1903,  until  an  attack  of  enteric 
fever  later  in  the  same  year,  for  which  he  was  in  hospital  in 
Japan  for  about  three  months.  He  never  regained  his  former 
health,  and  his  feet  were  often  swollen  at  night,  but  he  was 
able  to  work  until  July,  1908,  when  he  was  thrown  out  of  em- 


2.44  DISEASES  OF  THE  HEART 

ployment  by  the  failure  of  his  firm.  He  stayed  at  home  in 
fairly  comfortable  circumstances  until  he  procured  a  new 
situation  on  February  19,  1909.  In  the  early  part  of  February 
he  had  caught  cold,  and  he  was  feeling  "  run  down  "  when  he 
commenced  his  new  work.  This  entailed  a  daily  walk  of  four 
miles,  and  he  felt  exhausted  at  night  and  also  during  the  day 
when  walking  uphill;  but  though  he  steadily  became  weaker, 
he  continued  at  his  post  until  six  weeks  before  admission. 
when  he  was  compelled  to  go  to  bed.  His  cough,  accompanied 
by  a  sMght  mucoid  spit,  persisted  from  February  until  May. 
He  had  frequent  attacks  of  shivering  at  night  after  getting 
home ;  they  were  fairty  severe,  and  lasted  for  fifteen  to  twenty 
minutes,  and  he  felt  hot  after  he  got  into  bed,  and  often 
sweated  profusely  in  the  early  morning.  About  a  fortnight 
before  admission  his  right  forearm  and  elbow  became  sore  to 
the  touch  and  on  movement,  and  this  continued  for  a  few  days. 
Four  days  before  admission,  the  left  hip  and  ankle  became 
painful,  and  this  persisted. 

On  admission,  the  patient  was  found  to  be  a  thin,  pale, 
badly  nourished  man,  with  flabby  muscles  and  little  sub- 
cutaneous fat.  The  left  hip  and  ankle  were  painful  and  tender, 
and  there  was  a  small  tejider  area  of  induration  on  the  back  of 
the  left  forearm.  The  right  caK  was,  he  said,  painful;  but 
nothing  abnormal  could  be  detected.  There  were  several 
minute  ecchymoses  on  the  conjunctival  surface  of  the  right 
lower  eyehd,  and  a  fairly  large  one  on  the  conjunctiva  of  the 
left  bulb,  while  ophthalmoscopic  examination  revealed  a 
medium-sized  flame  shaped  haemorrhage  in  the  course  of  the 
left  superior  temporal  vein.  The  lungs  were  normal,  the 
tongue  was  clean,  the  digestion  good;  the  Hver  and  spleen 
were  shghtly  enlarged ;  the  urine  contained  a  small  amount  of 
albumin.  The  heart  was  but  little  enlarged,  though  there 
was  a  weU-marked  mitral  systohc  murmur.  The  pulse  was 
frequent,  regular,  small,  and  soft;  and  he  was  shghtly 
fevered  at  n^'ght.  The  leucocj-te  count  never  rose  above 
15,000. 

Progress  after  admission  was  slowly  but  continuously  in  the 
wrong  direction.  Many  embohsms  occurred,  chiefly  in  the 
Hmbs,  but  once,  at  any  rate,  in  the  spleen,  and  twice  in  the 


ACUTE  ENDOCARDITIS  245 

kidneys.  He  had  several  "faint  turns  "  of  a  feAv  minutes' 
duration  without  obvious  cause.  The  weakness  increased, 
and  after  the  middle  of  Juh'  oedema  was  more  or  less  continu- 
ally present  in  the  legs.  There  were  occasional  rigors  and 
generally  profuse  sweats  at  night.  On  August  25  a  left  hemi- 
plegia occurred,  and  he  died  on  August  29. 

The  pulse  during  the  patient's  residence  in  hospital  was 
always  regular  until  immediately  before  death ;  and  the  venous 
curves  were  normal,  save  that  the  a-c  interval  was  invariably 
prolonged,  measuring  about  0'25  second,  and  never  touching 
0-2  second  or  O'S  second. 

Post-7nortem  examination  revealed  an  acute  endocarditis 
of  the  mitral  valve.  Two  emboli  were  present  in  the 
right  middle  cerebral  arteries,  and  septic  infarctions  were 
present  in  the  left  kidney  and  the  spleen.  Erom  the  latter  the 
pneumococcus  and  Bacillus  coli  communis  were  ^isolated  in 
culture.     Blood-cultures  during  life  had  proved  sterile. 

The  mitral  valve  was  dilated.  Numerous  vegetations  were 
present  on  the  cusps,  some  small  and  wart-like,  others  long  and 
luxuriant.  The  endocardium  of  the  left  auricle  was  thick  and 
opaque,  and  a  few  minute  granulations  were  present  on  the 
contra-fossal  wall  immediately  above  the  valve;  the  endo- 
cardium at  this  point  was  notably  thickened.  There  was  no 
evidence  of  mural  impHcation  elsewhere. 

Microscopic  examiiuLtion  of  the  a.v.  node  and  bundle  re- 
vealed well-marked  congestion.  The  node  was  otherwise 
normal,  though  two  small  foci  of  round-cells  were  found  in 
the  auricular  muscle  in  its  immediate  vicinity.  The  bundle 
was  involved  in  three  separate  places  by  foci  of  the  "-ame  kind. 
The  first  was  of  small  size  and  was  situated  immediately  below 
the  node ;  the  second,  which  was  considerably  larger,  was  found 
a  httle  lower  down,  between  the  auricular  muscle  and  the 
bundle,  and  imphcated  both;  the  third,  of  fair  size,  occupied 
the  central  part  of  the  bundle,  and  occurred  inmiediately  above 
the  point  where  it  passed  through  the  central  fibrous  body. 
The  cehs  were  all  mononuclear  and  chiefl}'  l^-mphocytes .  The 
fibres  of  the  a.v.  bundle  seemed  normal,  save  in  the  immediate 
vicinity  of  the  two  larger  foci,  where  they  were  evidently  de- 
generate.    The  fibrous  tissue  of  the  bundle  was  not  excessive 


246  DISEASES  OF  THE  HEART 

in  amount.  The  s.a.  node  was  normal.  The  cardiac  muscle 
generally  showed  evidence  of  interstitial  myocarditis  in  an 
early  stage,  and  the  muscle  fibres  in  some  of  the  patches  were 
degenerate. 

In  some  cases  the  symptoms  point  to  the  existence  of  gross 
lesions  in  the  central  nervous  system,  and  the  diagnosis  may 
be  extremely  difficult  or  impossible.  An  old  man  was  admitted 
to  hospital  on  account  of  cerebral  symptoms  which  had  ensued 
•somewhat  rapidly,  and  as  an  aural  discharge  was  found  to 
exist,  the  mastoid  cells  were  exposed  and  drained,  but  without 
effect.  Post-mortem  examination  showed  that  the  symptoms 
were  due  to  embohc  occlusion  of  the  cerebral  vessels  associated 
with  a  mahgnant  endocarditis  of  the  mitral  valve.  The  otitis 
media  was  quiescent.  In  the  following  case  the  correct  diag- 
nosis was  considered  to  be  probable  on  account  of  the  sudden 
occurrence  of  the  cerebral  symptoms  and  their  association 
Avith  a  cardiac  lesion,  fever,  and  rigors.  The  significance  of 
the  occurrence  of  extra-systoles  and  nodal  rhythm  was  not  fully 
reaHzed  until  the  post-mortem  examination. 

Case  4. — The  patient,  a  man  aged  twenty -four,  was  ad- 
mitted into  hospital  on  July  15,  1909.  His  previous  health 
had  been  good,  save  for  attacks  of  measles  and  enteric  fever 
in  childhood;  but  he  was  often  troubled  with  gumboils,  and 
was  frequently  wetted  at  his  work. 

The  patient's  present  illness  dated  from  July  1,  when  he 
had  had  one  of  his  molars  extracted  on  account  of  a  gumboil 
from  which  he  had  suffered  for  a  day  or  two.  In  the  evening 
he  felt  sick  and  shivery,  and  probably  was  fevered.  Thes 
symptoms  continued,  and  on  the  afternoon  of  July  4  he  had 
a  definite  rigor.  On  the  7th  he  felt  better,  and  on  the  8th  he 
went  to  Ardrossan,  walking  from  the  station  to  the  house  at 
which  he  stayed  (a  distance  of  two  miles).  After  this  he  im- 
proved until  the  12th,  though  he  had  a  shght  cough  after  the 
6th,  with  discomfort  in  the  left  chest;  but  on  the  12th  he  had 
to  go  to  bed  as  the  pain  in  the  side  became  worse  and  was 
much  intensified  on  coughing.  The  left  arm,  too,  was  stiff, 
and  he  was  very  breathless  and  had  to  sit  up  in  bed  at  night. 
On  the  evening  of  the  13th  he  was  better,  and  able  to  sleep 
quietly  lying  down. 


ACUTE  ENDOCARDITIS  247 

On  July  14  the  man  felt  so  well  that  he  dressed  and  went 
downstairs,  which  he  did  without  any  difficulty  and  without 
assistance.  After  breakfast  he  sat  down  on  a  chair,  and  on 
attempting  to  rise  an  hour  later  found  that  his  legs  were  power- 
less and  "  had  no  feeling  "  in  them.  He  had  to  be  carried 
back  to  bed. 

On  admission,  the  patient  was  found  to  be  notabh'  emaciated, 
with  small  muscles  and  scanty  subcutaneous  fat.  His  com- 
plexion was  somewhat  sallow  and  his  expression  anxious, 
while  he  had  to  be  propped  up  in  bed  on  account  of  breathless - 
ness.  The  skin  was  hot  and  dry  and  there  was  a  little  oedema 
of  the  feet  and  slight  pitting  with  the  stethoscope  on  ausculta- 
tion over  the  cardiac  area.  He  was  shghtly  fevered  at  night. 
The  patient,  though  weak,  was  quite  clear  mentally,  spoke 
correctly,  and  answered  questions  accurately  and  sharply. 
He  had  little  power  in  his  legs,  but  was  able  to  pull  up  both 
knees,  though  he  was  unable  to  move  the  toes  of  the  right  foot. 
The  movements  were  more  free  on  the  left  side.  There  was 
considerable  anaesthesia  in  both  legs.  Power  was  perhaps  de- 
ficient to  some  slight  extent  in  the  left  arm,  but  in  the  right 
was  good,  and  sensation  seemed  normal.  The  right  pupil  was 
shghtly  smaller  than  the  left;  both  reacted  to  light  and  on 
accommodation. 

The  tongue  was  dry  and  coated,  many  of  the  teeth  were 
absent,  most  of  the  remainder  were  carious,  and  the  mouth 
generally  was  very  foul.  The  pulse  was  soft,  regular,  and  in- 
frequent. Palpation  of  the  apex-beat,  which  was  full  and 
widespread,  showed  that  ever}^  other  beat  was  missed  at  the 
radial,  the  cardiac  action  being  regularly  coupled.  A  systoHc 
murmur  was  audible  all  over  the  cardiac  area.  It  was  heard 
best  at  the  apex,  where  it  was  long  and  soft,  replacing  and 
running  out  of  the  first  sound ;  the  second  sound  was  not  audible 
here.  The  respirations  were  difficult  and  cycHc,  but  without 
any  full  apnoea.  A  consohdation  was  found  in  the  upper  part 
of  the  right  chest,  and  in  the  left  lower  axilla  friction  sounds 
were  audible.     The  urine  contained  a  trace  of  albumin. 

For  a  few  days  the  patient's  general  condition  improved 
slightly.  The  coupled  rhythm  ceased  on  the  16th,  and  he 
rested  fairly  well  at  night.     On  the  17th  movement  was  more 


248  DISEASES  OF  THE  HEART 

free  in  the  left  leg,  but  the  palsy  below  the  right  knee  persisted. 
About  midnight  on  the  18th  he  was  noticed  to  be  restless,  and 
was  found  to  be  semi-conscious  and  unable  to  say  more  than 
"Yes,"  and  there  was  a  well-marked  full  right  hemiplegia. 
He  gradually  became  weaker  and  more  comatose,  and  he  died 
from  cardiac  failure  on  Juh'  27. 

The  pulse  remained  "single  "  until  the  day  of  death,  when 
it  was  noticed  to  be  "  coupled  "  again  for  a  short  time.  The 
tracings,  which  were  obtained  in  this  case  during  the  coupled 
rhythm,  showed  that  there  was  a  shght  increase  of  the  a-c 
interval  (0"25  second)  with  the  first  or  larger  beat  of  the  couple, 
and  that  the  second  or  smaller  beat  was  a  ventricular  extra- 
systole  which  did  not  interfere  with  the  auricular  rhythm. 
Tracings  of  the  "  single  "  pulse  obtained  on  July  23  showed 
. „       a  regular  pulse  and  a 

°--     ac     as.     Q(z     ac      ftc    ac     ac    a.c     ac  , 

very  short  a-c  interval, 
measuring   httle    more 
?3^.<x?  "  "      than  0'05  second. 

,S^  Post-mortem  ex- 
amination revealed  an 
acute  ulcerative  endo- 
carditis of  the  mitral  valve,  engrafted  on  a  lesion  of  older 
standing.  The  upper  and  middle  lobes  of  the  right  lung  were 
sohd  from  a  somewhat  chronic  pneumonia,  and  there  were 
numerous  infarcts  in  the  spleen  and  kichiej's.  The  left  middle 
cerebral  artery  was  occluded  by  a  large  pale  embolus,  which 
resembled  the  vegetations  on  the  mitral  valve,  and  was  associ- 
ated mth  a  ver}-  extensive  softening.  Streptococci  were 
isolated  on  culture  from  the  spleen.  No  blood-cultures  were 
made  during  life. 

The  mitral  valve  was  stenosed,  the  cusps  being  notably 
shortened,  the  chordae  tendineae  short  and  thick,  and  the  tips 
of  the  papillar}^  muscles  fibrous.  There  was  well-marked 
evidence  of  fibrosis  spreading  upwards  from  the  bases  of  the 
cusps  in  the  direction  of  the  central  fibrous  body  of  the  heart. 
Enormous  soft  recent  vegetations  almost  occluded  the  valve, 
and  there  was,  in  addition,  extensive  ulceration  and  perforation 
of  the  anterior  mitral  cusp .  There  was  no  evidence  of  any  acute 
mural  endocarditis ;  but  the  endocardium  of  the  left  auricle 


viU^^KKUAiv^^^'' 


Fig.  134. — Nodal  Rhythm  (Case  1.). 


ACUTE  ENDOCARDITIS  249 

was  thick  and  opaque,  with,  a  special  area  of  thickening  about  as 
large  as  a  shilling  on  the  contra -fossal  wall  just  above  the  valve. 

Microscopic  examination  of  the  a.v.  tissues  revealed  con- 
siderable congestion  of  the  tissues  generally.  The  node  was 
the  site  of  a  profound  inflammatory  disturbance,  many  focal 
collections  of  round-cells  being  present,  as  well  as,  in  places,  a 
diffuse  infiltration.  The  fibres  of  the  a.v.  bundle  were  probably 
normal,  and  there  was  no  evidence  of  old-standing  fibrosis. 
The  walls  of  a  microscopic  artery  were  infiltrated  with  round- 
cells,  though  the  lumen  was  patent;  the  other  vessels  seemed 
normal.  The  intensity"  of  the  lesions  varied  at  different  levels, 
but  the  whole  of  the  node  was  more  or  less  affected.  The 
bundle,  on  the  other  hand,  was  not  implicated,  save  at  one  place 
immediately  below  the  node,  where  one  or  two  small  foci  in  the 
auricular  muscle  immediately  adjoining  it  passed  in  for  a  short 
distance  between  a  few  of  its  fibres.     The  s.a.  node  was  normal. 

There  was  a  weU-marked  myocarditis,  involving  both  ven- 
tricle and  auricle,  but  it  was  onh'  extreme  at  the  base  of  the 
mitral  valve,  and  in  the  auricular  sections  immediately  above 
the  node  itself. 

The  following  case  is  instructive  on  account  of  the  duration 
of  the  fever,  which  lasted  from  May  15  until  'July  28,  and  the 
ultimate  good  result.  The  fever  was  not  high,  and  only  once 
exceeded  103°  F.  The  mitral  and  the  aortic  valves  became 
affected  under  observation. 

Case  5. — D.  L.,  aged  twenty,  fireman,  was  admitted  on 
May  21,  1909,  complaining  of  pains  in  his  joints  of  six  days' 
duration.  His  previous  health  had,  on  the  whole,  been  good, 
save  for  an  attack  of  measles  when  a  child,  and  pneumonia  at 
the  age  of  sixteen.  He  was,  however,  hable  to  tonsillitis  until 
he  was  thirteen  years  of  age,  but  subsequently  it  had  ceased 
to  trouble  him.  Three  weeks  before  admission,  however,  his 
tonsils  again  became  acutely  inflamed,  and  he  was  in  bed  for 
a  week.  As  he  had  then  quite  recovered,  he  resumed  his  work, 
which  exposed  him  to  the  weather,  as  he  was  on  a  night  shift. 
On  the  evening  of  May  16  he  began  to  feel  pains  in  the  "  small 
of  his  back  " ;  on  the  evening  of  May  18  his  shoulders  began  to 
be  painful,  and  on  May  19  the  hips  were  affected,  and  he  was 
compelled  to  go  to  bed.     Xext  day  manj'  more  joints  were 


250  DISEASES  OF  THE  HEART 

implicated,  and  he  sweated  profusely.  On  admission  to 
hospital  he  M'as  found  to  be  a  well-nourished  man  of  good 
physique.  His  face  was  flushed  and  he  was  sweating  profusety, 
and  evidently  suffering  considerable  pain.  The  tongue  was 
furred,  the  mouth  foul,  and  both  tonsils  were  enlarged  and 
shghtlj'  inflamed.  The  knees  and  ankles,  the  wrists,  and  man}' 
of  the  phalangeal,  metacarpo-phalangeal,  and  metatarso- 
phalangeal joints  were  swollen  and  tender.  There  was  a  con- 
siderable amount  of  fluid  in  the  right  knee-joint.  The  other 
viscera  seemed  normal,  save  for  a  httle  catarrh  in  the  lungs 
The  arthritis  rapidly  became  less  acute,  but  persisted  in  one 
or  other  joint  until  the  end  of  June.  The  tonsillitis  persisted 
for  some  time  after  admission,  but  had  subsided  by  the  first 
week  of  June.  In  July,  however,  it  returned  and  persisted 
for  a  week,  and  again  in  the  last  week  of  November.  His 
general  condition  slowly  but  steadily  improved  after  acbnission, 
and  he  was  always  able  to  take  an  adequate  supply  of  nourish- 
ment. Bacteriological  examinations  of  the  blood  on  May  7 
and  July  11  were  negative.  The  leucocyte  count  reached  a 
maximum  of  lu,800  on  May  24.  The  cardiac  condition  never 
gave  rise  to  any  anxiety  from  the  sj^mptomatic  point  of  view, 
though  the  auscultatorj'  phenomena  indicated  grave  myo- 
cardial weakness.  The  apex  impulse  was  faint  and  was  not 
displaced.  On  auscultation  the  sounds  were  pure,  but  the 
first  sound  was  extremely  short  and  indistinct,  and  somewhat 
distant.  The  pulse  was  regular  and  fairly  full,  but  soft  and 
frequent.  The  first  sound  remained  short  and  distant,  but 
pure  for  about  a  fortnight,  after  which  it  began  to  lengthen 
from  the  addition  of  a  sj^stohc  murmur  of  mitral  distribution. 
Towards  the  end  of  July  a  short,  soft  diastohc  murmur  became 
audible  in  the  third  left  space  about  an  inch  from  the  sternal 
margin,  succeeding  an  emphatic  second  sound.  The  pulse- 
rate  only  reached  normal  hmits  at  the  end  of  July.  He  was 
allowed  out  of  bed  in  the  commencement  of  October,  and 
when  dismissed  home  on  Januar}^  24,  1910,  was  able  to  take  a 
fair  amoimt  of  exercise  and  to  walk  upstairs  without  any 
evident  discomfort.  The  heart  was  shghtly  enlarged,  and  the 
aortic  and  mitral  murmurs  persisted. 

Three  years  later  he  was  in  good  health,  and  playing  cricket 
on  occasion. 


CHAPTER  XX 
ACUTE  ENBOCARDITIS— Continued 

The  Diagnosis  o!  Acute  Endocarditis.^ — The  diagnosis  of  acute 
endocarditis,  though  often  self-evident,  may  be  at  times  ex- 
tremely difficult  or  even  impossible,  for  in  some  cases  the 
symptoms  are  general,  and  in  some  point  to  the  involvement 
of  other  organs  than  the  heart.  In  my  hospital  cases  the  symp- 
toms in  19  were  cardiac,  in  6  cerebral,  in  2  pulmonary,  and  in 
2  of  a  general  kind ;  one  patient  died  during  an  attack  of  chorea. 

In  the  majority  of  cases  fever  co-exists  (Fig.  135),  but  it  is  of 
no  special  type,  and  may  be  high  or  low,  and  continuous 
remittent  or  intermittent;  in  the  latter  case  rigors  often  occur. 
It  may,  too,  be  absent.  This  obtained  in  two  cases,  in  one  of 
which  it  was  perhaps  merely  a  measure  of  the  debility  of  the 
patient;  but  in  the  other  the  temperature  was  normal  during 
the  last  five  weeks  of  the  illness.  Fever  is  not  infrequently 
absent  during  the  acute  stages  of  rheumatic  endocarditis,  and 
the  temperature  may  even  be  subnormal ;  sometimes  the 
evening  temperature  rises  occasionally  to  99°  or  100°  F.  without 
any  obvious  cause;  or  a  subnormal  wave  of  "  pyrexia,"  lasting 
for  a  week  or  more,  may  be  apparent  on  the  chart  (Fig.  136.) 
Both  of  these  signs  are  significant. 

The  essential  feature  is  the  recognition  of  a  valvular  murmur, 
but  the  cardiac  sounds  may  be  unaccompanied  for  some  weeks 
(c./.  p.  234).  As  a  rule  the  valvular  disease  is  well  marked, 
but  previous  observation  may  be  wanting,  or  the  presence  of 
a  pre-existing  flaw  may  be  known,  and  the  separation  of  an 
acute  from  a  chronic  endocarditis  is  required.  Horder  has 
suggested  that  the  occurrence  of  embolism  and  the  isolation  of 
organisms  from  the  blood  are  almost  conclusive  evidence  of  an 
infective  endocarditis ;  but  while  this  is  probably  accurate,  it 

251 


252 


DISEASES  OF  THE  HEART 


ACUTE  ENDOCARDITIS 


253 


excludes  practically  all  the  cases  of  rheumatic  origin,  as  well 
as  manj'  others  in  which  blood-cultures  are  sterile,  and  thus 
restricts  the  recogni- 
tion of  the  disease. 
It  is  on  the  cardiac 
evidence  that  most 
reliance  must  be 
placed. 

I  would  again  em- 
phasize the  impor- 
tance of  the  pulse- 
rate  in  the  diagnosis . 
The  pulse-rate  may 
be  unduly  frequent  in 
fever,  from  emotion, 
from  cardiac  weak- 
ness, and  in  a  few 
diseases,  such  as 
phthisis,  exophthal- 
mic goitre,  rheuma- 
toid arthritis,  and 
diphtheria ,  apart 
from  cardiac  com- 
phcations.  But  the 
absence  of  these 
factors  can  be  readity 
determined  by  a  few 
observations,  and  in 
their  absence  a  fre- 
quent pulse -rate  is 
generall}^  due  to  an 
acute  cardiac  lesion. 
The  sudden  appear- 
ance of  irregularity 
has  a  similar  signifi- 
cance. Heart-block  is  so  generally  due  to  a  myocardial  fault 
that  its  appearance,  even  in  trivial  and  transient  degree,  suggests 
that  an  associated  endocarditis  is  acute  and  not  chronic  ;  and  the 
sudden  appearance  and  continuance  of  extra-systoles,  without 


Fig. 


133.— Chart   of  H.   O'K.,   Aged    12:  Acute 
Rheujiatisji;  Acute  EN^DDOAnorTis. 


Xote  siibnormnl  wave  of  "  p'/revi'i ' 
frequent  pulse-rate. 


and  uaiuly 


254  DISEASES  OF  THE  HEART 

obvious  pulmonary  complications  or  increase  of  cardiac  weak- 
ness, point  the  same  moral.  Nodal  rliytlmi  seems  to  be  most 
frequently  associated  with  an  acute  endocarditis.  Paroxys- 
mal tachycardia  and  auricular  fibrillation  have  no  particular 
significance. 

The  appearance  of  new  murmurs  is  as  a  rule  decisive,  and 
the  temporary  disappearance  of  murmurs  is  equally  suggestive, 
but  one  exception  must  be  remembered.  The  characteristic 
crescendo  murmur  of  mitral  stenosis  always  disappears  if 
auricular  fibrillation  or  nodal  rhythm  occurs ;  and  may  disappear 
in  partial  heart-block.*  If  a  sinus  rhythm,  continues,  the  con- 
clusion that  there  is  an  acute  lesion  is  probabl}^  always  correct. 

Embolism  is  of  frequent  occurrence.  It  may  of  course 
occur  in  chronic  endocarditis  from  the  separation  of  clots  in 
the  auricles,  but  it  is  often  multiple  and  recurrent  in  acute 
cases.  In  chronic  valvular  disease  puhnonary  embohsm  is 
more  common ;  in  acute  endocarditis  embolism  of  the  systemic 
arteries.  The  spleen  is  often  involved  (Horder,  47  cases)  and 
becomes  enlarged.  Occasionally  the  enlargement  is  great,  and 
in  one  of  my  cases  the  lower  border  reached  down  to  the 
umbihcus.  The  occurrence  of  an  infarct  may  be  acutely 
painful,  and  friction  may  be  audible  from  associated  peri- 
tonitis. Renal  infarct  is  also  common.  Gross  haematuria  was 
present  in  46  of  Horder's  cases  and  in  8  of  my  own;  but,  as 
Horder  points  out,  the  incidence  is  probably  greater,  for  the 
lesser  degrees  are  not  always  accompanied  by  macroscopic 
evidence  of  the  presence  of  blood.  The  brain  is  less  frequently 
affected,  but  the  cerebral  vessels  were  occluded  in  22  of  Horder's 
cases  and  in  3  of  my  own.  The  result  is  most  frequently 
softening,  but  haemorrhage  is  not  very  rare.  Meningitis 
occurred  in  4  of  my  cases. 

Infective  aneurisms  may  form.  Horder  reports  2  cases;  in 
one  the  aneurisms  were  multiple,  the  right  ulnar,  the  superior 
mesenteric,  and  the  hepatic  arteries  being  involved.  In  one 
of  my  cases,  a  boy  of  fourteen  years,  there  was  a  small  aneurism 
of  the  aorta  just  above  the  valves,  and  a  fusiform  aneurism, 
the  size  of  a  plum,  at  the  lower  end  of  the  left  iliac  artery. 
Both  the  artery  and  vein  were  occluded,  but  the  leg,  though 
*  W.  T.  Ritchie,  Edin.  Med,  Journ.,  1913,  vol.  x.,  N.S.,  p.  410. 


ACUTE  ENDOCARDITIS  255 

oedematous,  showed  no  signs  of  gangrene.  Cutaneous  mani- 
festations are  not  uncommon.  Petechial  eruptions  are  the 
most  frequent,  and  were  present  in  43  of  Horcler's  series  and 
in  6  of  my  own.  Subcutaneous  nodules  occurred  in  3  cases  in 
my  series,  and  persistent  erythema  and  urticaria  in  3  instances. 
Fugitive  tender  indurations  in  the  deeper  structures  have  a 
similar  significance. 

Gross  visceral  lesions  are  by  no  means  uncommon,  and  the 
co-existence  of  pneumonia,  pleurisy,  pericarditis,  etc.,  with  a 
valvular  murmur,  should  always  suggest  the  possibility  of  an 
endocarditis  being  acute. 

The  occurrence  of  a  leucocytosis  has  no  particular  diagnostic 
significance.  It  is  always  present  in  mahgnant  cases  save  in 
the  terminal  stages,  when  it  is  sometimes  absent;  but  it  is 
merely  evidence  of  a  septicaemia,  whose  presence  is  clearly 
shown  in  other  ways,  and  not  of  a  cardiac  infection.  A  count 
of  over  25,000  is  uncommon  in  the  rheumatic  forms. 

The  Prognosis  in  Acute  Endocarditis. — The  prognosis  in  acute 
endocarditis  is  clifiicult  to  assess.  The  majority  of  rheumatic 
cases  recover,  but  with  damaged  valves;  while  patients  from 
whom  positive  blood-cultures  have  been  obtained  usually  die. 

In  the  individual  case  the  risk  must  be  assessed  from  con- 
sideration of  the  usual  factors,  the  general  condition  of  the 
patient,  the  height  of  the  fever,  and  the  rapidity  of  the  pulse- 
rate  ;  and  the  prognosis  should  be  guarded  until  the  fever  has 
gone  and  the  pulse-rate  is  wdthin  normal  limits.  The  occur- 
rence of  rigors,  emboL'sm,  and  petechial  eruptions ;  the  appear- 
ance of  oedema,  and  progressive  dilatation  of  the  heart;  and 
alterations  in  the  rhj^thm  of  the  heart,  are  of  serious  signifi- 
cance. Comphcations,  such  as  pericarditis,  pleurisy,  and 
pneumonia  add  greatly  to  the  danger.  Dehrium  is  generally- 
the  immediate  precursor  of  death.  But  I  have  seen  patients 
recover  in  whom  each  of  these  symptoms  was  present,  and  I 
am  inchned  to  lay  most  stress  upon  the  general  nutrition  of 
the  patient.  If  this  can  be  maintained,  the  prognosis  is  never 
hopeless  ;  but  if  it  fails,  the  cardiac  infection  always  progresses. 

The  Treatment  of  Acute  Endocarditis. — ^There  is  no  specific^ 
treatment  of  acute  endocarditis,  for,  as  has  been  shown,  its 


256  DISEASES  OF  THE  HEART 

causes  are  diverse.  But  the  general  indications  are  clear,  and 
the  essential  part  of  the  treatment  is  rest. 

It  is  of  course  impossible  to  secure  physiological  rest  to  the 
heart,  for  life  ceases  when  the  heart  stops  beating ;  but  absolute 
confinement  to  bed  in  the  recumbent  posture  diminishes  the 
frequency  of  the  cardiac  contractions  and  insures  a  minimal 
blood-pressure ;  for  both  the  pulse-rate  and  the  blood-pressure 
are  appreciably  raised  even  by  sitting  up  in  bed.  Absolute 
rest  necessitates  full  nursing,  the  patient  doing  nothing  that 
can  be  done  for  him  by  a  nurse,  and  being  fed  and  washed 
and  dressed  with  as  little  voluntary  movement  as  is  possible. 
The  use  of  a  bed-pan  and  a  slipper  is  essential.  The  rest,  too, 
must  be  long  continued,  for  even  after  the  symptoms  have 
disappeared  and  the  curves  are  normal,  the  valves  are  infil- 
trated and  soft,  and  resolution  is  incomplete ;  and  the  size  of 
the  ultimate  scar  depends  upon  the  degree  of  movement  of 
the  cusps. 

In  too  many  instances  the  duration  of  the  rest  allowed  is  in- 
sufficient. It  is  impossible  to  assess  accurately  the  extent  of 
the  inflammation,  but  analogy  from  lesions  elsewhere,  such  as 
pneumonia  and  fractures,  shows  that  the  rate  of  resolution 
varies  considerably  in  individual  cases ;  and  the  only  wise  plan 
is  to  play  for  safety,  and  rather  to  prolong  the  rest  unnecessarity 
than  allow  exercise  at  a  time  when  it  will,  or  may,  cause  harm. 
The  effects  of  exertion  on  the  incidence  of  endocarditis  in  acute 
rheumatism  are  well  known,  and  the  lesions  are  less  common 
and  less  severe  in  cases  where  the  severity  of  the  arthritis  has 
driven  the  patient  at  once  to  bed,  as  contrasted  with  the  milder 
cases  where  the  patient  has  been  able  to  go  about  for  days  or 
even  weeks. 

Absolute  rest,  then,  is  indicated  until  aU  symptoms  have 
disappeared,  and  the  rate  and  rhythm  of  the  pulse  are  normal . 
When  this  has  occurred,  the  patient  may  be  allowed  to  sit  up 
in  bed  for  short  periods,  the  size  of  the  area  of  cardiac  duhiess 
and  the  pulse-rate  being  carefully  watched ;  and  the  periods 
may  be  gradually  increased  if  no  untoward  result  follows.  He 
should,  however,  be  confined  to  bed  for  at  least  two  months 
longer,  and  for  another  month  merely  moved  on  to  a  couch; 
before  he  is  allowed  to  stand  up  and  walk.     Restrictions  as  to 


ACUTE  ENDOCARDITIS  257 

exercise  must  be  continued  for  at  least  three  to  six  months 
longer,  and  violent  exercise,  such  as  games,  interdicted  for  a 
year  or  so  afterwards. 

Massage  is  useful  during  the  period  of  rest,  and  may  be 
commenced  as  soon  as  the  patient  is  allowed  to  sit  up,  the 
massage  being  at  first  slight  and  of  short  duration,  and  only 
increased  very  gradually.  Every  effort,  too,  should  be  made 
to  improve  the  general  health,  and  plenty  of  fresh  air  and  a 
variety  of  food  utilized  with  this  in  view.  In  suitable  weather 
much  time  may  be  spent  out  of  doors. 

The  results  obtained  by  these  means  are  surprising.  One 
patient,  aged  forty  when  I  saw  him,  had  a  heart  so  full  of  mur- 
murs that  no  valve  could  be  pronounced  sound,  but  its  size  was 
normal.  He  was  a  lawyer  in  busy  practice  who  took  much  exer- 
cise, and  he  had  never  had  any  cardiac  symptoms  since  his 
attack  of  acute  rheumatism  twenty  years  before.  But  at  that 
time  he  was  for  six  months  in  bed  and  for  six  months  on  a 
couch,  and  he  was  not  allowed  to  walk  quickly  for  another 
year.  .  -'^' 

From  the  clinical  standpoint  cases  of  endocarditis  may  be 
divided  into  three  groups:  (1)  Those  which  are  of  rheumatic 
origin ;  (2)  those  in  which  blood-cultures  reveal  the  presence  of 
bacteria;  and  (3)  those  in  which  blood-cultures  are  sterile, 
though  they  seem  to  have  no  connection  with  acute  rheu- 
matism. 

1.  The  incidence  of  endocarditis  in  acute  rheumatism,  as 
gauged  by  statistics  in  the  literature,  does  not  seem  to  be 
appreciably  lessening,  so  that  it  appears  that  sahcylate  treat- 
ment has  little  effect  in  preventing  this  complication.  Every- 
one knows  how  difficult  it  is  in  some  cases  to  overcome  the 
tendency  of  the  arthritis  to  relapse  in  this  disease ;  and  most 
of  us  have  watched  cases  of  rheumatic  endocarditis  progress 
steadily,  notwithstanding  sahcylate  treatment.  It  has,  in 
consequence,  been  suggested  that  the  failure  of  the  salicylates 
indicates  a  non-rheumatic  infection.  The  inference,  however, 
does  not  seem  justifiable,  for  cases  of  malaria  or  syphilis  may 
run  a  mahgnant  course  in  spite  of  treatment  by  quinine  or 
mercury ;  and  the  obvious  conclusion  is  that  acute  rheumatism 
may  run  a  malignant  course.     A  progressive  lesion  merely 

17 


258  DISEASES  OF  THE  HEART 

indicates    a    severe    infection,    not    necessarily    different    in 
nature. 

The  action  of  large  doses  of  salicylates  upon  the  heart, 
slowing  its  rate  and  weakening  its  action  and  lowering  the 
blood-pressure,  has  been  held  to  contra-indicate  their  adminis- 
tration in  cases  where  the  heart  is  involved.  If  there  is  any 
evidence  of  cardiac  weakness,  the  contention  is  obviously 
sound,  but  in  its  absence  the  drug  should  be  exhibited,  as 
apart  from  the  question  of  a  specific  action  upon  the  infection, 
the  lessening  in  rate  and  the  lowering  of  blood-pressure  are 
beneficial  to  the  local  lesion.  Large  doses  are,  however, 
unwise,  but  60  to  90  grains  may  be  given  daily  to  an  adult  in 
combination  with  equal  dose^,  of  sodium  bicarbonate.* 

Sahcylate  poisoning  is  comparatively^  infrequent.  The 
lesser  degrees  are  most  frequently  observed  in  patients  who  are 
suffering  from  high  blood-pressure  and  defective  elimination. 
In  any  case  attention  should  be  paid  to  the  smallest  mani- 
festations of  intolerance,  and  the  drug  should  be  intermitted 
if  they  appear. 

2.  The  isolation  of  bacteria  from  the  blood  necessarily  raises 
the  question  of  specific  treatment,  and  it  seems  reasonable  to 
administer  the  corresponding  antiserum  in  these  cases,  even 
though  one  must  as  a  rule  employ  a  polyvalent  serum,  and  not 
one  specially  prepared  from  the  particular  organism.  The 
results  which  have  been  obtained,  however,  are  extremely 
disappointing,  and  only  one  or  two  cases  have  been  recorded 
in  which  recovery  ensued.  My  own  experience  has  been  uni- 
formly unsatisfactory. 

Vaccine  treatment,  too,  has  had  equally  poor  results,  and  it 
seems  extremely  doubtful  if  good  results  will  ever  be  obtained 
in  this  way.  The  production  of  antibodies,  which  is  the  aim 
of  this  treatment,  takes  place  in  disease  in  response  to  the 
presence  of  bacteria  or  of  their  products,  and  may  fail  to  be 
sufficient  if  the  infection  is  local  and  absorption  minimal;  or 
if  the  infection  is  intense  and  the  defensive  processes  are  over- 
powered.    Of  all  the  conceivable  sites  of  infection,  the  endo- 

*  The  administration  of  alkali  in  an  amount  sufficient  to  render  the  urine 
alkaline,  and  the  prevention  of  constipation,  obviates  the  risk  of  salicylate 
poisoning  (Lees),  which  is  perhaps  due  to  an  acid  intoxication. 


ACUTE  ENDOCARDITIS  259 

cardium  is  surely  that  most  certain  to  produce  a  general 
intoxication,  and  I  fail  to  comprehend  how  in  these  general 
"  arterial  "  septicsemias  an  additional  dose  of  the  poison  can  be 
of  benefit  to  the  patient. 

In  four  cases,  however,  recovery  has  ensued  after  treatment 
of  this  kind,  and  although  the  satisfactory  result  may  not  have 
been  due  to  the  specific  treatment,  the  uniformly  fatal  ter- 
mination in  cases  in  which  such  treatment  has  not  been  tried 
should  perhaps  encourage  further  experiments.* 

3.  In  the  third  group  the  indications  for  treatment  of  a 
specific  kind  are  lacking.  The  salicylates  have  generally  been 
already  tried  and  have  failed,  and  serum  or  vaccine  treatment 
are  negatived  by  the  failure  to  isolate  a  bacterium.  General 
treatment  of  the  kind  that  has  been  already  laid  down — com- 
plete rest,  fresh  air,  an  abundant  dietary  (solid  food  can  often  be 
well  digested  by  fevered  patients) — is  of  course  already  in  action. 

It  seems  probable  that  in  many  of  these  cases  continual 
reinfections  of  the  blood-stream  (and  of  the  valves)  are  occur- 
ring from  local  septic  foci  which  may  exist  in  different  situa- 
tions .  The  tonsils  are  often  large  and  deeply  pitted ;  the  nose 
or  middle  ears  are  septic;  or  the  teeth  are  carious  and  the 
mouth  is  foul.  The  urethra,  the  bladder,  the  uterus,  etc..  may 
be  infected.  The  influence  of  such  septic  foci  in  the  production 
of  a  visceral  infection  is  difficult  to  estimate,  but  an  impression 
is  gradually  arising  that  they  are,  at  any  rate,  of  greater  im- 
portance than  has  hitherto  been  recognized;  and  that  little 
good  result  is  likely  to  occur  unless  the  reinfections  of  the 
valves  are  stopped  by  eradication  of  the  source  of  the  re- 
infection. The  general  condition  of  the  patient,  or  the  nature 
of  the  primary  focus,  may  make  it  difficult  to  secure  asepsis,  but 
I  have  on  two  occasions  seen  permanent  improvement  ensue 
in  cases  which  seemed  to  be  progressing  downhill,  after  removal 
of  enlarged  tonsils ;  and  on  one  occasion  a  great,  though  un- 
fortunately only  temporary,  relief  after  removal  of  some  dozen 
carious  teeth. 

*  Sir  James  Barr,  W.  Blair  Bell,  and  Captain  S.  R.  Douglas,  Lancet^ 
London,  1907,  vcl.  i.,  p.  499.  A.  Latham  and  E.  L.  Hunt,  Proc.  Royal  Soc. 
Med.,  London,  1910,  vol.  iv.  (Clinical  Section),  p.  14.  G.  Jochmann,  Berlin 
Klin.  Woch.,  1912,  p.  436.  H.  Hemstead  and  T.  J.  Horder,  Lancet,  London,. 
1913,  vol.  i.,  p.  10. 


260  DISEASES  OF  THE  HEART 

From  the  preventive  point  of  view,  in  any  case,  such  measures 
are  urgently  required,  and  no  "  rheumatic  "  patient  should  be 
allowed  to  harbour  septic  foci,  even  in  the  absence  of  cardiac 
disease. 

Many  drugs  have  been  advocated  in  these  cases — horse 
serum  (to  supply  complement),  arsenic,  mercury,  quinine, 
silver  in  the  colloidal  form,  etc.  I  have  once  or  twice  thought 
that  coUargol  injected  intravenously,  and  applied  as  Crede's 
ointment  to  the  skin  of  the  trunk,  was  responsible  for  improve- 
ment, but  in  most  cases  it  has  no  effect.  The  most  important 
factor  is  probably  the  digestion;  and  so  long  as  the  nutrition 
of  the  patient  can  be  maintained  or  improved,  recovery  may 
be  hoped  for;  with  anorexia  or  digestive  disturbance  the  pro- 
gress is  invariably  in  the  wrong  direction.  Cardiac  weakness 
must  be  combated  by  the  usual  means,  but  its  appearance  in 
acute  endocarditis  is  always  of  grave  significance. 


CHAPTER  XXI 
CHRONIC  VALVULAR  DISEASE 

The  Lesions. — Chronic  valvular  disease  of  the  heart  interferes 
in  greater  or  less  degree  with  the  proper  working  of  the  valves, 
and  thus  imposes  an  extra  strain  upon  the  heart ;  but  as  the 
lesions  differ  in  their  grade  and  are  not  necessarily  confined 
to  the  cusps  but  may  involve  the  "  cyhnder  "  as  well,  the 
ultimate  result  varies  in  different  cases,  and  the  interference 
with  the  valvular  action  may  be  considerable  or  of  little 
moment. 

The  conditions  which  are  found  post-mortem  are  of  various 
kinds.  The  normal  soft,  pliable,  translucent  appearance  is 
lost,  and  the  cusps  are  hardened,  stiffened,  and  opaque,  the 
change  being  in  some  cases  uniformly  distributed  throughout, 
and  in  others  confined  to,  or  most  extreme  at,  the  free  margins 
or  the  lines  of  attachment.  Calcareous  and  atheromatous 
deposits  are  not  uncommon,  and  although  usually  merely  an 
addition  to  a  general  change,  are  sometimes  an  isolated  lesion 
in  a  fairly  normal  cusp.  The  calcareous  deposits  are  occa- 
sionally so  large  that  by  their  mere  bulk  they  interfere  with  the 
proper  action  of  the  valve,  and  may  prevent  its  closure  or 
obstruct  its  orifice  (Fig.  137). 

The  cusps  may  be  shortened  or  adherent  to  each  other ;  and 
while  shortening  produces  incompetence,  adhesion  causes  nar- 
rowing of  the  orifice ;  the  two  results  frequently  co-exist.  The 
ultimate  result  varies.  Sometimes  the  cusps  are  more  or  less 
uniformly  joined  together,  and  a  funnel  or  dome-shaped  ap- 
pearance is  produced ;  and  sometimes  the  longitudinal  shrinkage 
is  extreme,  and  a  diaphragm  results  (Fig.  138).  The  chordae 
tendineae,  and  even  the  musculi  papillares,  may  be  imphcated 
in   the  fibrosis  of  the  mitral  valve,  and  the  whole  apparatus 

261 


262 


DISEASES  OF  THE  HEART 


may  be  welded  together  into  a  single  mass  (Fig.  139).  The 
orifice  is  often  greatly  narrowed,  and  may  be  rounded  or  linear 
or  stellate. 

In  many  cases  warty  outgrowths  of  varying  size  and  con- 
sistence are  visible  at  the  margins  of  the  cusps  ;  in  others  erosion 
and  loss  of  substance  are  the  main  feature,  and  the  edges  are 
puckered  and  uneven.  The  line  of  attachment  may  be  eroded 
and  part  of  a  cusp  may  be  freely  mobile  in  the  blood-stream ; 
or,  if  it  is  calcified,  project  stiffly  into  the  lumen.  These  results 
are  most  common  in  the  aortic  valve,  for  destruction  of  the 
chordae  tendineae  of  the  mitral  valve  usually  produces  so  great 

an  interference  with  the  cardiac 
action  that  death  ensues  during 
the  acute  stage. 

The  cusps  may  be  perforated 
through  their  substance.  This  is 
most  commonly  the  result  of  acute 
endocarditis,  but  sometimes  follows 
severe  muscular  effort  or  an  external 
trauma.  Those  pathological  per- 
forations must  not  be  confounded 
with  fenestration  of  the  cusps,  a 
congenital  defect  of  no  importance, 
which  does  not  interfere  with  the 
action  of  the  valves.  The  dis- 
tinction is  easy,  as  the  fenestras  are  situated  close  to  the 
margins  of  the  cusps,  and  on  surfaces  which  are  opposed  during 
closure;  while  the  edges  are  unaltered,  and  neither  thick  nor 
hard.  In  the  former  the  cusps  are  abnormal,  and  the  per- 
forations are  at  the  centre  of  the  cusps  or  near  their  attach- 
ments. 

In  the  majority  of  chronic  aortic  defects  the  edges  of  the 
cusps  are  more  or  less  inverted ;  in  rare  instances  the  edges  are 
everted.*  In  the  latter  case  (Fig.  140)  the  curtains  are  usually 
voluminous  rather  than  shortened,  but,  though  thickened,  are 
so  soft  that  they  fall  downwards  towards  the  ventricle  and 
impose  no  obstacle  to  the  regurgitation  of  blood ;  there  is  rarely 
necrosis  or  ulceration,  and  vegetations,  if  present,  are  generally 


Fig.  137. — Calcaeeotjs  Infil- 
tration ?  OF  Aortic  Valve 
(R.  I.  Museum). 


Cowan,  Glasgow  Med.  Journ.,  1902,  vol.  Iviii.,  p.  198. 


CHRONIC  VALVULAR  DISEASE 


263 


scanty  and  small.  Microscopic  sections  show  that  the  con- 
nective tissue  of  the  cusps  is  loose  and  degenerate,  with  patches 
of  leucocytic  infiltration  which  are  most  numerous  at  the  base 
of  the  valve  and  in  the  aortic  wall;  the  vessels  here  show  in- 
flammatory changes  and  a  narrowed  lumen  interfering  with  the 


Fig.  138. — Teaxsverse  Section  of  Heart,  viewed  from  above 
(W.  I.  Museum). 

The  mitral  valve  is  greatly,  and  the  tricuspid  valve  slightly,  stenosed.     Both 
auricles  are  greatly  dilated. 

nutrition  of  the  valve  and  producing  degeneration  of  the  new- 
formed  connective  tissue. 

The  lesions  frequently  extend  beyond  the  valve.  The  waU 
of  the  aorta  is  often  affected,  showing  either  a  diffuse  thicken- 
ing or  a  patchy  change ;  the  orifice  may  be  so  greatly  dilated 
that  even  cusps  of  normal  size  would  be  insufficient  to  occlude 
it.      The  mitral    orifice,   on  the  other  hand    is  more  often 


264 


DISEASES  OF  THE  HEART 


CHORD/E     TENDlNE/€ 


ANTERIOR.     CUSP 


MUSCULI     PAPILLARES 

Fig.  139.— Ftjnnel-Shaped  Miteal  Endocarditis  (W.  I.  Museum). 

The  mitral  cusps,  the  chordse  tendinese,  and  the  musculi  papillares  are  all  welded 

together. 


CHRONIC  VALVULAR  DISEASE  265 

narrowed  than  dilated,  for  the  inflammatory  spread  into  the 
muscle  in  the  course  of  cicatrization  leads  to  narrowing.  The 
auricular  wall  may  be  affected. 

Valvular  defects  are  rarely  pure.  Stenosis  is  almost  always 
associated  with  some  degree  of  incompetence ;  and  conversely 
incompetence  is  generally  accompanied  by  some  degree  of 
narrowing.  In  aortic  cases  incompetence  is  the  rule,  and 
stenosis  is  minimal  and  rarely  extreme.  In  mitral  cases 
stenosis  is  the  rule,  and  incompetence  co-exists ;  for  the  ana- 
tomical division  of  the  mitral  valve  into  an  anterior  and  a 
posterior  cusp  is  inaccurate,  as  it  is  reallj^  a  circidar  curtain 


Fig.  140. — Flabby  "Wash-Leather"  THiCKExrs:G  or  Aortic  Valve,  which 

WAS    NOTABLY   InCOMPETEXT   (W.    I.  MuSEUM). 

with  special  developments  of  certain  parts;  and  if  it  is  uni- 
formly involved,  the  lumen  is  necessarily  narrowed  by  the  con- 
traction of  the  scar  tissue. 

The  close  proximity  of  the  valves  to  particular  structures  is 
an  important  factor  in  the  ultimate  progress  of  the  case.  The 
orifices  of  the  coronary  arteries  are  frequently  involved  in 
aortic  disease,  and  the  a.v.  node  and  bundle  are  often  damaged 
in  mitral  and  in  aortic  lesions.  The  interference  mth  the 
nutrition  of  the  heart  produced  by  the  former,  and  the  dis- 
turbance of  the  cardiac  rhythm  entailed  by  the  latter,  imprint 
special  characters  upon  the  sj^mptoms  of  these  diseases. 

The  Etiology  of  Chronic  Valvular  Disease.  —  There  is  con- 
siderable difficulty  in  determining  the  precise  causes  of  chronic 
valvular  lesions.  More  than  one  cause  is  frequently  active; 
the  effects  of  different  causes  are  very  similar ;  the  chronicity 


266 


DISEASES  OF  THE  HEART 


of  the  disease  prevents  accurate  observation  of  its  progress ;  and 
the  ultimate  result  depends  on  the  site  of  the  affection  rather 
than  on  the  nature  of  the  cause. 

Chronic  valvular  disease  may  follow  (1)  acute  endocarditis; 
(2)  syphihs;  or  (3)  mechanical  strain;  or  may  be  (4)  merely  a 
part  of  a  general  cardio-vascular  degeneration,  or  (5)  a  defect 
of  development. 


Fig.  141. — IMiteal  Endocarditis,  showing  a  Large  Healed  Scar  on  the  Wall 
OF  THE  Left  Auricle  (c/.  Fig.  131)  (R.  I.  Museum). 


1.  Acute  Endocarditis. — A  priori  it  seems  probable  that  a 
slight  acute  endocarditis  may  resolve  completely,  but  patho- 
logical data  are  necessarily  lacking,  and  the  cHnical  evidence  is 
insufficient  to  prove  the  point.  In  the  majority  of  cases  the 
wound  heals  in  course  of  time,  but  resolution  is  imperfect  and 
a  scar  is  left  behind,  which  from  the  constant  movements  of 
the  parts,  is  larger  than  it  would  have  been  if  it  had  been 
situated  on  a  less  mobile  site.  Necrotic  lesions  of  course 
cannot  be  replaced,  so  that  in  practically  every  case  of  acute 
endocarditis  a  valvular  defect  is  left.   If  the  lesion  is  small, 


CHRONIC  VALVULAR  DISEASE  267 

the  mechanical  defect  may  be  minimal,  but  the  damage  makes 
the  valve  more  vulnerable,  and  more  liable  to  be  seriously 
injured  by  causes  which  would  produce  little  effect  upon  a 
healthy  valve.  The  free  margins  of  the  cusps  are  most 
-affected,  and  the  lesions  may  be  confined  to  these  parts,  or 
may  involve  the  whole  of  the  cusp. 

2.  Syphilis. — The  effects  of  syphihs  are  only  gradually 
l»eing  appreciated  at  their  true  value.  The  specific  arterial 
lesions  have  but  recently  been  distinguished ;  a  syphiUtic  scar 
upon  a  valve  closely  resembles  those  produced  by  other  causes ; 
^nd  the  chronic  disease  can  only  be  recognized  by  the  presence 
■of  other  syphihtic  stigmata, though  the  acute  lesions  are  distinc- 
tive. These  are  well  shown  in  Fig.  142.  The  patches  on  the 
■aorta  are  characteristic,  and  the  thick  yellow  nodules  upon 
the  aortic  and  mitral  cusps  are  exactly  similar.  The  damage  is 
more  widespread  than  would  appear  from  mere  inspection  of 
the  surface ;  and  the  cut  surface  of  the  cusp  to  the  left  of  the 
•drawing  shows  a  widespread  thickening.  Syphihtic  nodules 
tend  to  break  down  in  their  centre,  and  the  resultant  scar 
leads  to  shortening  and  puckering  of  the  cusps .  The  valvular 
■disease  may  occur  at  any  stage  of  the  disease,  and  though  most 
•common  as  a  late  sequel,  may  also  obtain  comparatively  early 
if  treatment  is  defective.  Accurate  data  are  difficult  to  pro- 
cure, but  in  one  case  where  the  patient  died  mth  aortic  and 
mitral  disease,  the  symptoms  of  cardiac  distress  appeared  two 
years  after  the  chancre,  and  two  years  before  death.  No 
specific  treatment  had  been  undergone.  The  patient  was 
incKned  to  athletic  exercises,  and  the  symptoms  may  have 
I)een  accelerated  by  physical  exertion. 

3.  Mechanical  Strain. — The  relations  of  mechanical  injury  to 
chronic  valvular  disease  are  equally  difficult  to  assess,  though 
isolated  cases  have  proved  beyond  doubt  that  acute  lesions 
may  be  produced  in  this  way.  Sir  Cfifford  Allbutt*  quotes 
many  examples.  A  healthy  man,  aged  thirty-six,  was  crushed 
between  a  cart-wheel  and  a  post,  and  died  a  few  days  after- 
wards ;  the  healthy  aortic  valves  had  been  torn  away  from  the 
healthy  aorta.  A  man,  aged  nineteen,  had  an  aortic  cusp 
ruptured  from  the  free  margin  to  the  base  by  a  blow  upon  the 

*  Allbutt's  "  System,"  1909,  vol.  vi.,  p.  425. 


268 


DISEASES  OF  THE  HEART 


chest.     A  man,  aged  twenty,  fell  from  a  scaffold  and  developed 
well-marked  aortic  regurgitation.     And  in  a  certain  number 


Fig.  142. — Syphilitic  Aortitis,  with  Involvement  of  Aortic  and  IMitrai* 
Valves  (R.  I.  Museum). 

of  cases  the  severe  strain  of  some  physical  exertion  has  been 
so  rapidty  followed  b}^  serious   cardiac  symptoms   that  the 


CHRONIC  VALVULAR  DISEASE  269 

association  seems  clear.  A  porter,  for  example,  who  was  Kfting 
a  heavy  trunk  on  to  a  barrow,  suddenly  became  exceedingly 
breathless,  and  when  I  saw  him  a  few  days  later,  was  the 
subject  of  well-marked  aortic  regurgitation.  No  other  cause 
than  the  strain  could  be  discovered.  But  such  cases  are  rare, 
and  in  most  the  evidence  points  to  valvular  disease  being 
antecedent  to  the  trauma,  which  produced  gross  results  in  con- 
sequence of  some  local  weakness. 

Two  other  groups  of  cases  of  mechanical  strain  require  con- 
sideration. In  some  occupations  (moulders,  draymen,  riveters, 
et  alii)  severe  physical  exertion  is  constantly  undertaken, 
with,  in  consequence,  high  blood-pressure  during  the  period  of 
stress;  and  in  some  diseases  (arterio-sclerosis,  chronic  renal 
disease)  the  blood-pressure  is  constantly  above  normal.  The 
question  of  the  influence  of  an  intermittent  or  a  constant  high 
blood-pressure  upon  the  valves  naturally  arises. 

There  is  no  doubt  that  men  in  arduous  employments  grow 
old  before  their  time ;  the  Clyde  shipbuilders  are  rarely  in  active 
work  after  the  age  of  fifty-five ;  and  the  main  damage  falls  upon 
the  heart  and  the  arteries.  But  the  habits  of  these  men  are 
often  loose.  Sweating  labour  is  often  associated  with  the  con- 
sumption of  large  quantities  of  alcohol;  and  syphihs  and  other 
infections  and  intoxications  not  infrequently  co-exist ;  so  that 
it  is  difficult  to  ascertain  the  exact  value  of  the  mechanical 
factor. 

The  influence  of  intermittent  strain  can  hardh/  be  determined 
by  pathological  examination,  though  microscopic  haemorrhages 
and  local  scars  have  been  found  in  such  cases.  A  correct 
appreciation  of  the  frequency  of  its  action  can  only  be 
gauged  by  clinical  data  on  the  large  scale.  But  there  is 
already  much  information  available  with  regard  to  the  occur- 
rence of  chronic  valvular  disease  in  cases  of  high  blood-pressure, 
and  it  has  been  found  that  the  valves  are  very  frequently 
damaged. 

The  connection  between  mitral  and  renal  disease  was  first 
noticed  by  Barclay  in  1848,  and  several  writers  have  in  the 
interval  investigated  the  question  from  post-mortem  data. 
Goodhart  found  that,  of  97  cases  of  renal  cirrhosis,  47  had  mitral 
lesions  ;  while  of  215  cases  of  (clinically)  primary  mitral  disease, 


270  DISEASES  OF  THE  HEART 

31  had.  cirrhotic  kidneys.  Newton  Pitt  found  that,  of  542 
cases  of  renal  cirrhosis,  33  had  mitral  stenosis,  and  that  33  per 
cent,  of  115  cases  of  mitral  stenosis  had  renal  cirrhosis.  In  a 
series  of  335  cases  of  renal  fibrosis  (capsules  adherent ;  surface 
more  or  less  granular)  reported  by  Fleming  and  myself,*  60 
had  organic  disease  of  the  mitral  valve  (17"9  per  cent.),  and  of 
93  cases  of  mitral  disease  60  had  fibroid  kidneys.  It  seems 
certain,  too,  that  the  association  is  not  accidental,  for  in  a 
corresponding  series  of  807  cases,  in  which  the  kidneys 
were  not  fibroid,  only  33  (4  per  cent.)  had  organic  mitral 
disease. 

The  relationship  between  mitral  and  renal  disease  is  not 
always  the  same. 

1.  In  some  cases  it  seems  clear  that  the  cardiac  lesion  is 
primary.  A  man  who  died  at  the  age  of  twenty-one  had 
suffered  from  chorea  at  the  age  of  three ;  the  mitral  valve  was 
notably  hard  and  deformed,  while  the  kidneys  were  only  slightly 
affected.  A  woman  who  died  at  the  age  of  forty-eight  had 
suffered  from  acute  rheumatism  at  twenty-two;  the  mitral 
lesion  was  extensive  and  the  interstitial  nephritis  "early"; 
while  a  woman  who  died  at  the  age  of  thirty-five  had  had 
several  attacks  of  acute  rheumatism  before  twenty-eight ;  and 
her  kidneys,  though  granular,  were  still  large.  In  all  three 
cases  the  symptoms  were  cardiac. 

'  It  seems  improbable  that  the  renal  lesion  is  due  to  chronic 
venous  congestion  as  has  been  suggested,  for  if  that  were  the 
case,  the  liver  should  suffer  as  frequently  as  the  kidneys ;  but 
in  our  series  of  93  cases  of  organic  mitral  disease,  the  kidneys 
were  affected  in  60  and  the  liver  in  but  9.  The  causes  of  renal 
cirrhosis  are  still  unknown,  but  there  is  considerable  evidence 
in  favour  of  the  view  that  it  may  be  due  to  faulty  metabolism 
and  the  consequent  irritation  of  the  kidneys  by  abnormal 
substances  which  are  excreted  in  the  urine ;  and  chronic  venous 
congestion  of  the  digestive  organs  is  extremely  likely  to  derange 
their  proper  action,  and  is  not  infrequently  accompanied  by 
gastro-intestinal  catarrh,  which  will  exert  its  own  special 
action. 
^     2.  But  in  another  group  of  chronic  mitral  cases  the  usual 

*  Quart.  Journ.  of  Med.,  1912,  vol.  v.,  p,  309. 


CHRONIC  VALVULAR  DISEASE 


271 


causes  of  acute  endocarditis  are  conspicuously  absent.  A 
woman  who  died  at  the  age  of  forty-five  would  not  admit 
having  had  any  illness  whatever  before  the  onset  of  that  which 
ultimately  proved  fatal.  A  woman,  aged  forty-three,  had  had 
measles  and  scarlatina  in  childhood,  but  had  always  been 
healthy  until  a  few  winters  before  her  death,  when  she  became 
hable  to  bronchitis  and  short  of  breath  on  exertion.  A  man, 
aged  forty-seven,  had  had  no  previous  iUness,  with  the  ex- 
ception of  an  attack  of  "  gastric  "  fever  at  the  age  of  fourteen. 
And  there  are  a  small  number  of  cases  on  record  in  which 
mitral  stenosis  has  been  observed  to  develop  in  the  absence  of 
all  acute  disease  (Sansom).  It  is  generally  agreed  that  the 
most  frequent  causes  of  those  chronic  cases  are  arterio- 
sclerosis and  chronic  nephritis,  and  in  these  three  cases  the 
kidneys  were  more  or  less  granular  and  their  capsules  were 
adherent. 

Huchard  has  outhned  the  process  by  which  the  lesion  is 
produced.  The  vessels  of  the  valve  are  frequently  degenerate, 
their  lumen  is  diminished,  and  minute  haemorrhages  are  not 
uncommon.  As  a  result  the  overlying  endothelium  is  lost 
and  fibrin  is  deposited  upon  the  uncovered  surface;  and  the 
constant  movements  of  the  part  produce  a  "  callus  "  which  is 
large  and  out  of  proportion  to  the  original  lesion.  Kennedy, 
too,  has  investigated  the  point  and  finds  that  the  basal  portions 
of  the  mitral  cusps  are  almost  always  thickened  and  fibroid  in 
chronic  renal  disease  (Figs.  143,  144,  145). 

It  thus  seems  evident  that  in  some  cases  the  renal  lesion  is 
the  cause  of  the  mitral  one,  but  it  is  improbable  that  this  is 
the  common  sequence.  It  is  true  that  the  incidence  of  mitral 
disease  in  cases  of  renal  fibrosis  is  much  greater  than  in  cases 
where  the  kidneys  are  normal,  but  the  incidence  is  much 
greater  in  women  than  in  men,*  a  fact  which  suggests  that  the 
connection  often  arises  in  other  ways. 

3.  Mitral  and  renal  disease  may  conceivably  be  due  to  the 
same  cause,  and  though  actual  proof  of  this  association  is 


Renal  Fibrosis. 

Mitral  Disease. 

Per  Cent. 

Men 
Women 

201 
134 

27 
33 

13-4 
24-6 

272 


DISEASES  OF  THE  HEART 


lacking,  the  evidence  in  its  favour  is  suggestive.  Newton  Pitt 
and  Sansom  maintained  that  acute  endocarditis  and  nephritis 
might  both  originate  during  the  puerperium,  and  so  initiate  the 
chronic  disease,  and  Rolleston  has  suggested  that  they  might 
result  from  syphilis.  Acute  syphihs  at  the  present  day  rarely 
causes  death,  and  its  real  importance  as  a  cause  of  chronic 
mischief  is  apt  to  be  obscured  by  its  chronicity.  I  have  ob- 
served one  case  in  which  both  the  kidneys  and  the  cardiac 


Fig.  143. — Chronic  Renal  Disease:  Patchy  Thickening  towards  the  Base 
OF  the  Mitral  Valve  (R.  I.  Museitm). 


valves  were  affected.  The  patient  had  contracted  a  chancre 
four  years  before,  for  which  he  had  not  received  specific  treat- 
ment. The  arteries  were  extensively  diseased,  the  aortic  valve 
was  notably  deformed  and  grossly  incompetent,  the  mitral 
valve  was  dilated  and  the  cusps  shortened  and  thickened,  and 
the  cortex  of  the  kidneys  was  slightly  atrophied  and  their 
surface  somewhat  granular.  Scarlatina,  too,  is  a  not  infre- 
quent cause  of  acute  endocarditis  and  acute  nephritis,  and 
might  affect  the  heart  and  the  kidneys  simultaneously. 


CHRONIC  VALVULAR  DISEASE 


273 


Some  recent  papers  have  thrown  a  new  hght  upon  the  matter. 
The  subacute  forms  of  acute  endocarditis  from  which  Horder 
and  Libman  have  so  frequently  isolated  streptococci  are  very 
often  accompanied  by  glomerular  changes  in  the  kidneys  of 
embohc  origin.  An  interstitial  leucocytic  infiltration  occurs 
in  the  vicinity  of  the  affected  tufts,  while  the  tubules  are  only 
slightly  affected.     Most  of  the  patients  in  whom  blood-cultures 


/ 


/ 


Fig.  144. — Chronic  Renal  Disease:  Diffuse  Thickening  of  the  Base, of  the 
MiTKAL  Valve  (R.  I.  Museum). 


have  been  positive  have  died,  and  only  a  few  have  recovered ; 
but  it  seems  probable  that  a  mild  infection  of  the  same  kind 
is  not  uncommon,  though  blood-cultures  are  negative,  and  that 
healing  takes  place,  leaving,  however,  a  chronic  valvular 
defect  and  a  chronic  renal  lesion.* 

*  P.  Baehr,  Amer.  Journ.  Med.  Sci.,  1912,  vol.  cxliv.,  p.  317.     J.  F.  Gaskell, 
Journ  of  Pathol.,  1911-12,  vol.  xvi.,  p.  287.     E.  Libman,  Zoc.  cit. 

18 


274 


DISEASES  OF  THE  HEART 


The  association  between  aortic  and  renal  disease  is  also 
striking,  and  h,as  been  recognized  for  many  years .  MacDonald  * 
has  examined  post-mortem  data  upon  this  point  and  found  that 
of  200  cases  of  renal  fibrosis,  34  (17  per  cent.)  had  organic  lesions 
of  the  aortic  valve,  while  in  25  more  the  valves  showed  "  com- 
pensatory thickening."  Of  32  cases  of  aortic  disease,  25  (78 
per  cent.)  had  renal  fibrosis,  which  was  present  in  18  (81  per 


Fig,  145. — Chronic  Eenal  Disease:  Diffuse  Thickening  in  Mitral  and  Aortic 
Valves  and  the  Adjacent  Endocardium  (R.  I.  Museum). 

cent.)  of  22  cases  in  which  both  aortic  and  mitral  valves  were 
diseased. 

The  varying  relationships  which  exist  between  mitral  and 
renal  disease  may  also  occur  between  the  latter  and  aortic 
disease,  but  it  seems  probable  that  the  renal  lesion  is  less  fre- 
quently secondary  to  the  cardiac  disease. 

4.  General  Car dio- Vascular  Degeneration. — The  influence  of 
a  generalized  cardio-vascular  degeneration  in  the  production 
of  chronic  valvular  disease  has  been  in  part  considered  in  the 
*  Glasgoiv  Med.  Journ.,  1914. 


CHRONIC  VALVULAR  DISEASE  275 

preceding  paragraphs.  No  clear  distinction  can  be  drawn 
between  the  heart  and  the  arteries.  The  intimal  Hning  is 
exactly  similar,  and  the  valves  are  merely  a  double  layer  of 
endothelium  enclosing  a  delicate  connective  tissue;  and  in 
cases  of  chronic  arterial  disease  comparable  lesions  are  often 
found  on  the  cusps.  The  aortic  valve  suffers  most  frequently, 
but  atheromatous  and  calcareous  plaques  are  not  uncommonly 
found  on  the  anterior  mitral  flap,  and  presumably  own  the 
same  causes  as  the  arterial  disease.  The  mitral  cusps,  at  any 
rate,  possess  arteries  of  their  own,  and  any  interference  with 
their  lumen  will  necessarily  entail  defective  nutrition  of  the 
valves  and  produce  lesions  comparable  to  those  which  occur  in 
the  great  vessels  from  such  causes. 

5.  Congenital  Defects. — Congenital  defects  of  the  heart  are  not 
common,  and  though  they  generally  involve  the  great  vessels 
or  the  muscular  septa,  in  many  instances  the  valves  also  are 
affected.  The  aortic  and  pulmonary  cusps  may  thus  be  more 
or  less  numerous  than  usual,  or  represented  by  a  diaphragm 
or  a  cone-shaped  funnel.  The  orifice  may  be  involved;  one 
vessel  may  be  narrowed  and  the  other  widened;  or  one  alone 
may  persist.  The  defects  arise  during  the  division  of  the 
truncus  arteriosus  into  the  pulmonary  artery  and  the  aorta 
vera.  Many  such  cases  have  been  recorded,  but  in  Abbott's 
valuable  article  in  Osier's  "System"  only  four  examples  of  de- 
velopmental malformation  of  the  mitral  valve  are  recorded. 
It  seems  almost  incredible  that  the  auriculo-ventricular  septum 
is  so  rarely  abnormal,  and  much  more  probable  that  the  nature 
of  the  defect  has  not  been  recognized.  It  is  well  known  that 
valves  which  are  congenitally  defective  are  not  infrequently 
attacked  by  acute  endocarditis,  and  this  may  so  disguise  the 
abnormahty  that  its  real  nature  is  not  appreciated.  A  con- 
genital defect  may  be  the  cause  of  some  of  these  valvular 
lesions,  which  seem  to  own  none  of  the  more  usual  causes. 

The  Causes  o£  Aortic  and  Mitral  Disease. — The  tables  pub- 
lished by  Lockhart  Gillespie  and  by  Grant  Andrew,  showing 
the  age  and  sex  incidence  of  chronic  valvular  disease,  contain 
important  indications  as  to  its  etiology,  though  the  conclu- 
sions arrived  at  are  only  approximately  correct,  as  the  figures  are 


276 


DISEASES  OF  THE  HEART 


merely  those  obtained  at  the  time  of  admission  to  hospital,  and 
show  neither  the  age  at  which  the  disease  originated  nor  the 
age  at  death,  but  merely  that  at  which  serious  symptoms  were 
present. 


Age. 

Aortic.                              j 

JIlTRAL.                                                1 

Gillespie. 

Andrew. 

M:wDonald. 

Gille 

-pie. 

Aud 

•ew. 

MacDonald. 

M.      K. 

M.      F. 

M.       F. 

M. 

F. 

M. 

F. 

M.     F. 

1  to    9 

— 

2     — 

— 

17 

10 

8 

10 

1        1 

10  ..  19 

13      2 

22       5 

6    — 

78 

114 

76 

118 

8      10 

20  ,.  29 

43     15 

44     18 

2      4 

92 

150 

84 

118 

5     12 

30  „  39 

66     14 

65     17 

11       2 

106 

96 

93 

96 

7     12    1 

40  „  49 

95     13 

76     14 

12       3 

81 

63 

85 

76 

6     29    , 

50  ,.  59 
60  ..  69 

70 

|l26     13/ 
11 

354     57 

48       8 

13     — 
5     — 

|210 
13 

86 1 
4 

75 

37 

1       9 

i 

273     63 

49       9 

597 

523 

465 

468 

29     73 

LocKHAKT  Gillespie:  Edin.  Hospital  Reports,  1898,  vol.  v.,  p.  293. 
Grant  Andrew:  Age  Incidence,  Sex,  and  Comparative  Frequency  in  Disease 
1909. 

The  causes  of  aortic  and  mitral  lesions  are  evidently  different, 
for  while  the  majority  of  aortic  cases  occur  after  the  age  of 
forty,  the  majority  of  mitral  cases  occur  before  that  age;  and 
while  aortic  disease  is  much  more  prevalent  in  men  than  in 
women,  mitral  disease  affects  the  sexes  in  approximately  equal 
proportions .  The  chief  incidence  of  aortic  disease  in  men  is  after 
forty ;  in  women  between  twenty  and  fifty.  Mitral  disease  is  most 
c  ommon  in  men  in  the  fourth  decade,  and  in  women  in  the  third. 

The  causes  which  we  have  considered  are  Hkely  to  be  active 
at  particular  periods  of  hfe.  Developmental  defects  of  course 
occur  during  intra-uterine  life;  acute  endocarditis  is  most 
common  in  adolescence  and  in  early  adult  life;  syphihs  and 
physical  strain  in  early  manhood ;  and  high  blood-pressure  and 
cardio-va^cular  degeneration  after  middle  life.  Aortic  disease 
in  men  thus  seems  likely  to  be  mainly  due  to  the  influence  of 
syphilis  and  physical  strain ;  while  in  women  acute  endocarditis 
should  be  an  important  factor.  Mitral  disease  in  men  seems 
likely  to  be  mainly  due  to  acute  endocarditis  and  high  blood- 
]">ressure  and  general  degenerative  changes  ;  in  women  to  acute 
endocarditis. 


CHRONIC  VALVULAR  DISEASE  277 

David  MacDonald  has  examined  my  hospital  records  from  this 
point  of  view.  The  numbers  are  small  (aortic  cases,  58 ;  mitral 
cases,  102)  and  the  numerical  fallacy  must  be  borne  in  mind; 
but  no  other  observations  are  available,  and  the  conclusions 
on  the  whole  agree  with  those  deduced  from  the  more  general 
considerations . 

Congenital  Defects. — Obvious  congenital  defects  are  not  in- 
cluded in  his  series. 

1.  Acute  Endocarditis — Aortic  Cases. — A  history  of  "rheu- 
matism "  was  given  in  20  cases  (34  per  cent.);  in  13  it  seemed 
to  be  clearly  acute  rheumatism ;  in  2  it  was  described  as  "  grow- 
ing-pains," in  one  of  which  it  was  associated  with  chorea;  in 
the  other  cases  its  nature  was  indefinite.  In  16  cases  other 
infections  were  recorded:  scarlatina,  6;  measles,  3;  smallpox, 
pneumonia,  2 ;  typhus  fever,  influenza,  pleurisy,  1 ;  but  the  hst 
is  obviously  incomplete.  Smallpox,  measles,  and  typhus 
fever  are  rarely  accompanied  by  endocarditis,  so  that  the 
incidence  of  endocarditis  in  this  series  is  not  Ukely  to  be 
greater  than  30  (51  per  cent.),  and  in  all  probability  is 
less . 

Mitral  Cases. — A  history  of  "  rheumatism  "  was  given  in  68 
cases  (66  per  cent.) ;  in  47  it  seemed  to  be  clearly  acute  rheu- 
matism; in  9  it  was  subacute;  in  4  it  was  described  as  "grow- 
ing-pains " ;  in  1  it  was  gonorrhceal.  Three  patients  had  had 
chorea,  2  recurring  tonsilhtis,  and  2  had  suffered  from  muscular 
rheumatism.  In  25  cases  other  infections  are  recorded: 
Measles,  8;  scarlet  fever,  5;  scarlet  fever  and  measles,  5;  in- 
fluenza, 5;  typhoid  fever  and  measles,  diphtheria,  1.  The  list, 
again  is  obviously  incomplete.  ^Excluding  measles,  typhoid 
fever,  and  diphtheria,  the  incidence  of  acute  endocarditis  in 
this  series  is  not  hkely  to  be  greater  than  83  (81  per  cent.),  and 
in  all  probabihty  is  less . 

2.  Syphilis — Aortic  Cases. — In  10  cases  (17  per  cent.)  the 
patients  had  suffered  from  syphilis,  but  the  figures  certainly 
minimize  the  incidence,  as  the  evidence  of  the  Wassermann 
reaction  shows  that  the  proportion  should  be  larger.  Routine 
examinations  have  only  recently  been  instituted  in  my  wards, 
but  the  test  was  positive  in  9  out  of  13  cases ;  and  in  18  out  of 


278  DISEASES  OF  THE  HEART 

22  cases  collected  from  the  literature.*  Aneurism,  too,  which 
is  so  frequently  syphilitic  in  origin,  co-existed  in  9  of  my  aortic 
cases. 

Mitral  C'ases. — Syphilis  was  known  to  have  existed  in  only 
1  case.     Aneurism  co-existed  in  1  case. 

3.  Mechanical  Strain. — No  examples  of  gross  trauma  occurred 
in  the  series.  The  influence  of  a  continuously  high  blood- 
pressure,  too,  cannot  be  estimated  in  aortic  disease,  for  in  aortic 
regurgitation  it  occurs  as  a  necessary  result  of  the  valvular 
disease,  and  independently  of  any  associated  defect  else- 
where. In  mitral  disease  a  high  blood-pressure  is  often  present 
(36  out  of  59  cases),  but  in  many  cases  the  evidence  points  to 
the  elevation  occurring  subsequently  to  the  onset  of  the  cardiac 
lesion.  In  some  cases,  however,  it  seems  probable  that  the 
connection  is  reversed,  and  that  the  valvular  flaw  is  secondary 
to  changes  arising  elsewhere.  The  association  has  already 
been  considered  at  length  on  p.  271. 

4.  General  Cardio- Vascular  Degeneration. — The  evidence  of 
vascular  disease  is  not  infrequently  well  marked  in  cases  of 
chronic  valvular  affections.  The  brachial  arteries  are  often 
notably  tortuous,  and  the  radials  distinctly  thickened,  and  one 
may  be  doubtful  whether  to  catalogue  a  patient  as  a  cardiac  or 
an  arterial  case.  In  some  the  lesions  may  be  very  extensive, 
A  man,  aged  flfty- seven,  was  admitted  into  my  wards  com- 
plaining of  a  cough,  accompanied  by  spit,  and  of  great  breath- 
lessness,  which  had  ensued  flve  weeks  previously  after  a  chill. 
The  heart  was  considerably  enlarged,  and  double  aortic  murmurs 
were  audible,  as  well  as  that  of  mitral  incompetence ;  the  pulse 
was  notably  shotty.     The  whole  of  the  arterial  tree  and  most  of 


Cases  of  Aortic 
lusuflBcieney. 

W 

assermann  Test, 
Pofcitive. 

*Clough  1 
Collins  and  Sachs  2  . , 

..       9     .. 
..     13     .. 

Aortic  and  Mitral 
Disease. 

..       6 
..     12 

5      .. 

..       2 

Mitral  Disease. 

11       .. 

2 

1  Johns  Hopkins  Hasp.  Bull.,  1910,  vol.  xxi.,  p.  70. 

a  Trans.  Assoc.  Amer.  Phys.,  1909,  vol.  xxiv.,  p.  351.    Cf.  Longcope,  Journ. 
Amir.  Med.  Assoc,  1910,  vol.  liv.,  p.  118. 


CHRONIC  VALVULAR  DISEASE  279 

the  accessible  veins  were  diseased.  Skiagrams  disclosed  a 
general  dilatation  of  the  aortic  arch  without  any  localized 
aneurism;  and  the  temporal,  facial,  brachial,  radial,  ulnar, 
superficial  volar,  femoral,  posterior  tibial,  and  dorsaHs  pedis 
arteries  were  thickened,  tortuous,  and  hard,  though  no 
calcification  was  apparent  on  X-ray  examination.  Ophthalmo- 
scopic examination  showed  that  the  retinal  arteries  were 
normal. 

The  superficial  veins  of  the  legs  were  large  and  varicose,  and 
the  capillaries  were  dilated  and  visible  halfway  up  the  legs,  the 
dilatation  being  maximal  in  the  feet.  The  veins  of  the  arms 
were  large  and  tortuous  ;  and  an  anastomotic  vein  as  large  as  a 
lead  pencil  crossed  the  hypogastrium  from  groin  to  groin,  the 
flow  of  blood  being  from  left  to  right. 

The  patient  was  a  moulder  by  trade,  and  had  been  intem- 
perate in  early  life,  though  for  a  number  of  years  he  had  been 
an  abstainer ;  the  Wassermann  reaction  was  frankly  positive. 
His  symptoms  were  only  cardiac  in  part.  The  right  dorsahs 
pedis,  though  easily  felt,  did  not  pulsate,  and  several  scars  on 
the  toes  remained  as  evidence  of  gangrene  which  had  occurred 
two  years  before  admission.  The  oedema  which  was  present 
on  admission  w^as  trivial  in  degree  and  rapidly  disappeared,  and 
might  quite  well  have  resulted  from  the  varicosity  of  the  veins. 
Cheyne-Stokes  breathing  and  a  copious  albuminuria  showed 
that  the  kidneys  were  grossly  diseased. 

His  early  symptoms,  however,  were  cardiac.  Eive  years 
previously  he  had  strained  himseK  when  at  work,  and  had  had 
to  lie  up  for  several  weeks  on  account  of  breathlessness  on 
exertion,  oedema  and  prsecordial  pain;  and  he  had  fainted  re- 
peatedly during  the  intervening  years.  During  his  convales- 
cence in  the  ward  he  overexerted  himself  on  one  occasion  and 
the  oedema  recurred,  and  the  liver  and  the  heart  became 
definitely  enlarged,  so  that  the  cardiac  reserve  was  evidently 
small.  From  the  general  point  of  view,  however,  the  arterial 
mischief  seemed  the  essential  lesion,  the  aortic  cusps  being 
probably  affected  as  a  secondary  result. 

One  must  bear  in  mind  that  the  presence  of  arterial  disease 
does  not  necessarily  indicate  that  the  cardiac  lesion  is  its 
result,  for,  as  already  mentioned,  renal  fibrosis  and  general 


280 


DISEASES  OF  THE  HEART 


arterio-sclerosis  are  not  infrequently  secondary  effects  of 
chronic  valvular  disease.  The  whole  history  of  the  case  must 
be  investigated  and  the  evidence  carefully  weighed  before  a 
decision  is  made  and  a  prognosis  given,  for  the  primary  arterial 
group  are  not  far  distant  fromi  their  end  when  the  cardiac 
valves  have  become  incompetent,  and  have,  in  consequence, 
a  worse  outlook  than  cases  in  whom  the  valvular  disease  is 
primary.  But  in  both  definite  arterial  damage  is  always 
serious,  for  it  may  kill  rapidly  and  with  but  little  warning. 

Exact  figures  as  to  the  incidence  of  vascular  disease  were 
unfortunately  not  available  in  this  series. 


The  special  incidence  of  mitral  disease  in  the  female  sex 
between  the  ages  of  ten  and  thirty  requires  further  considera- 
tion. It  occurs  at  a  period  of  life  when  acute  endocarditis  is 
most  frequent,  and  is  thus  most  likely  to  be  due  to  rheumatic 
conditions.  Grant  Andrew's  figures,  however,  show  that  acute 
rheumatism  is  more  common  in  males  than  in  females  at  those 
ages,  and  there  is  no  evidence  that  endocarditis  occurs  more 
frequently  in  one  sex  rather  than  in  the  other  during  acute 
rheumatism.  The  explanation  is  probably  to  be  found  in  its 
association  with  chorea,  which  is  three  times  as  common  in 
girls  as  in  boys.* 

MacDonald's  conclusions  thus  seem  to  support  those  which 
were  deduced  from  more  general  considerations.  Acute  endo- 
carditis is  the  most  common  cause  of  chronic  mitral  disease. 
Syphilis  and  physical  stress  are  probably  of  almost  equal  im- 


Age. 

Acute  Rheumatism. 

Chorea. 

Grant  Andrew. 

MaoDouald. 

[  Grant  Andrew. 

1 

JIacDonald. 

M.           F. 

M.            F. 

i\r.         F. 

M.           F. 

1  to    9 

7             5 

2          2 

11         45 

2          5 

10  „  19 

77         82 

23        23 

46       134 

11        27 

20  „  29 

132        95 

31         18 

1         17 

—          2 

30  „  39 

69         32 

19         12 

!       4        - 



40  „  49 

24         19 

6          4 

— 



50  .,  59 

13           3 

1           1 

— 

— 

60 

2         

— 

— 

— 

324      236 

82         60 

62       196 

13        34 

CHRONIC  VALVULAR  DISEASE  281 

portance  to  acute  endocarditis  in  causing  aortic  disease.  And 
both  aortic  and  mitral  disease  may  occur  in  later  life  associated 
with  chronic  renal  and  arterial  disease.  The  last  group  may 
arise  in  several  ways ;  from  high  blood-pressure,  from  arterial 
lesions,  or  from  the  chronic  intoxication  which  accompanies 
all  chronic  renal  disease ;  all  three  factors  may  be  active  at  the 
same  time. 

A  special  group  may  be  mentioned  here.  Chronic  valvular 
disease  is  not  uncommon  in  women  who  have  borne  many 
children,  and  is  often  accompanied  by  renal  mischief.  It 
seems  probable  that  in  some  instances  the  orgin  is  to  be 
ascribed  to  parturition  producing  coincident  lesions  in  both 
heart  and  kidneys. 

In  individual  cases  the  cause  of  the  valvular  mischief  is 
sometimes  obscure,  and  all  the  usual  factors  may  seem  to  be 
absent.  An  example  was  recently  brought  to  my  notice  by  a 
medical  friend  whose  sister  had  been  found,  on  a  routine  ex- 
amination for  insurance,  to  have  well-marked  mitral  stenosis. 
Her  age  was  twenty-four,  and  the  most  careful  investigations 
failed  to  ehcit  any  evidence  of  antecedent  illness  beyond  a  mild 
attack  of  measles.  She  had  never  suffered  from  rheumatism, 
tonsillitis,  chorea,  or  scarlet  fever,  was  httlehable  to  "colds," 
and  had  always  enjoyed  excellent  health.  Her  general  develop- 
ment and  nutrition  were,  if  anything,  above  the  average,  and  a 
developmental  defect  seemed  the  most  probable  explanation. 
In  another  case,  in  whom  mitral  stenosis  was  discovered  at 
the  age  of  sixteen,  the  girl  had  never  suffered  from  any  illness. 


CHAPTER  XXII 

THE  SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE 

The  symptoms  of  the  various  forms  of  chronic  valvular 
disease  differ  in  their  incidence  and  their  degree  rather  than  in 
their  nature,  and  may  conveniently  be  considered  together 
irrespective  of  the  lesions  with  which  they  are  most  commonly 
associated.  The  special  significance  of  particular  symptoms 
will  be  considered  subsequently. 

The  Causes  o!  Symptoms. — Chronic  valvular  disease  is  not 
necessarily  accompanied  by  symptoms  of  cardiac  discomfort, 
and  many  individuals  with  valvular  flaws  are  able  to  lead  lives 
of  average  activity  without  distress.  A  valvular  flaw,  of 
course,  imposes  an  extra  strain  upon  the  heart,  but  compen- 
satory arrangements  are  made  which  overcome  the  particular 
difficulty.  In  aortic  stenosis,  for  example,  the  lumen  of  the 
valve  is  narrowed,  and  the  flow  of  blood  into  the  aorta  is,  in 
consequence,  impeded.  But  if  the  ventricle  contracts  more  for- 
cibly, and  the  rate  of  flow  through  the  valve  is  sufficiently 
increased,  the  normal  quantity  of  blood  will  enter  the  aorta  in 
the  normal  period,  and  the  disability  will  be  overcome.  Under 
ordinary  circumstances,  the  heart  works  at  less  than  half  its 
full  power,  the  reserve  being  retained  to  meet  the  extra  strain 
of  physical  exertion,  and  so  any  small  degree  of  valvular  incom- 
petence is  readily  compensated. 

The  additional  work  thrown  upon  the  heart  causes  hyper- 
trophy of  the  muscular  fibres  which  are  concerned,  in  exactly 
the  same  way  that  regular  exercise  causes  hypertrophy  of  the 
systemic  muscles ;  so  that  the  additional  work  is  carried  on 
easily  and  well.  But  there  is  a  limit  to  hypertrophy,  and  even 
when  it  is  considerable,  the  power  that  can  be  developed  is 
never  so  largely  in  excess  of  that  ordinarily  required  as  in  a  normal 

282 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     283 

heart.  The  reserve  is  only  30  or  20,  or  10  per  cent,  instead  of 
the  normal  50,  and  what  James  Mackenzie  calls  "the  field  of 
response  "  is,  in  consequence,  limited.  A  man  may  become 
breathless,  for  example,  during  a  hard  game  of  tennis,  though 
able  to  walk  about  without  discomfort.  He  may  only  be  able  to 
walk  up  a  flight  of  stairs  which  formerly  he  could  run  up ;  he 
may  only  be  able  to  walk  quietly  on  the  level;  or  he  may  be 
incapable  of  any  exertion,  though  perfectly  comfortable  when 
seated  on  a  chair.  The  difference  is  merely  a  matter  of  degree, 
but  the  response  of  the  heart  to  demands  for  increased  activity 
is  more  or  less  insufficient. 

With  a  stationary  lesion  of  trivial  degree  and  good  general 
nutrition,  the  field  of  response  may  be  large  and  ample,  and  the 
patient's  disabihties  trivial  or  imperceptible,  and  many  indi- 
viduals live  for  years  without  discomfort.  Sir  William  Broad- 
bent  has  recorded  the  case  of  a  doctor,  aged  forty,  in  busy 
country  practice,  who  had  had  aortic  regurgitation  for  twenty - 
six  years.  Sir  William  Osier  reported  the  case  of  a  lady,  aged 
sixty-three,  who  had  mitral  regurgitation  from  the  age  of 
fifteen,  but  nevertheless  possessed  a  healthy  family  of  eleven 
children  !  Balfour  knew  a  hale  old  gentleman  of  eighty-eight 
who  had  had  a  mitral  leak  for  sixty-six  years  ! !  And,  per- 
sonally, I  know  two  men,  aged  forty -four  and  thirty-four,  with 
well-marked  congenital  defects,  who  have  never  suffered  from 
any  cardiac  symptoms. 

With  a  stationary  lesion  and  ample  compensation,  symptoms 
then  are  absent,  and  continue  absent  indefinitely;  but  in  the 
majority  of  cases  they  make  their  appearance  in  course  of  time. 
Their  appearance  is  generally  due  to  the  activity  of  some  new 
factor,  originating  in  the  heart  itself  and  affecting  the  valves 
or  the  muscle ;  or  in  some  other  viscus  and  producing  a  disturb- 
ance of  its  action  which  indirectly  affects  the  heart.  ^^ 

The  valvular  lesion  may  be  'progressive,  and  the  mechanical 
difficulty  may  steadily  increase.  Congenital  disease  is  as  a 
rule  associated  with  so  great  a  disturbance  of  the  circulation 
that  it  is  incompatible  with  normal  growth.  Many  of  these 
children  die  shortly  after  birth;  some  survive  for  a  few  years, 
but  with  stunted  growth  and  imperfect  nutrition,  and  readily 
succumb   to  accidental  infections.     But  a  congenital  defect 


284  DISEASES  OF  THE  HEART 

which  has  not  interfered  with  normal  growth  or  nutrition, 
and  has  not  produced  smy  symptoms  before  adult  Hfe  is 
attained,  is,  in  one  respect,  the  valvular  lesion  which  has  the 
best  prognosis,  for  it  is  one  which  is  not  progressive,  and  in 
which  no  recurrence  of  the  causal  factor  can  arise.  The  de- 
generative va  Ivular  lesions  associated  with  widespread  arterial 
disease  are,  on  the  other  hand,  essentially  progressive  in  their 
nature,  and  as  years  pass  the  defect  necessarily  becomes 
greater,  and  the  cardiac  reserve  becomes  smaller  and  smaller. 
The  lesions  which  are  due  to  acute  endocarditis  are  interme- 
diate in  their  tendency.  A  rheumatic  scar  of  course  contracts 
for  a  period  of  months  or  3'ears,  but  not  indefinitely,  and  an  old- 
standing  chronic  lesion  is,  in  consequence,  a  stationary  one. 
But  acute  rheumatism  tends  to  recur  and  is  pecuharly  apt  to 
reinfect  damaged  valves,  so  that  the  cause  may  again  come 
into  action  and  the  lesion  may  again  become  progressive. 
Muscular  hypertrophy  jnay  attain  to  enormous  size  (a  heart 
weighing  53  ounces  has  been  recorded),  but  there  is  a  limit  to 
its  development,  and  a  progressive  lesion  in  course  of  time 
produces  mechanical  difficulties  which  no  possible  hypertrophy 
can  compensate.  With  a  progressive  lesion  cardiac  failure 
sooner  or  later  ensues. 

^^h.e  symptoms  may  be  due  to  failure  of  the  cardiac  muscle. 
An  individual's  adaptability  to  his  environment  is  always 
relative  rather  than  absolute;  we  cannot  add  a  cubit  to  our 
stature;  and  the  most  carefully  regulated  course  of  physical 
exercises  may  fail  to  produce  an  athlete  if  he  comes  of  poor 
stock.  This  vital  factor  is  almost  incalculable.  A  long-lived 
stock  means  a  good  family  vitaUty,  and  the  heart  of  a  member 
of  such  a  family  is  more  likely  to  develop  satisfactory  hyper 
trophy,  if  it  is  required,  than  that  of  one  belonging  to  a  family 
whose  members  usually  die  in  early  life.  Muscular  failure 
arises  in  various  ways,  and  may  arise,  too,  in  hearts  which 
have  no  valvular  defect. 

The  general  nutrition  of  the  patient  is  always  a  matter  of 
importance,  for  the  cardiac  muscle  shares  in  any  general 
weakness.  In  mild  cardiac  failure  a  vicious  circle  is  often 
estabhshed.  Shght  venous  stasis  occurs,  the  gastro-intestinal 
tract  becomes  congested,  digestion  and  absorption  become  de- 


SY^IPTOMS  OF  CHROmC  VALVULAR  DISEASE     285 

fective,   the  general  nutrition  and  the  cardiac  nutrition  are 
impaired,  and  the  cardiac  insufficiency  is  augmented. 

The  cardiac  nutrition  alone  may  be  defective.  This,  too, 
is  of  common  occurrence,  for  it  is  dependent  almost  wholly 
upon  the  integrity  of  the  coronary  arteries.  And  if,  as  is  often 
the  case,  the  blood-supply  is  lessened  by  narrowing  of  these 
arteries,  at  their  origin  or  in  their  course,  the  cardiac  power  may 
be  notably  decreased. 

The  cardiac  rhythm  may  be  disturbed,  and  all  the  abnormal 
rhythms  of  themselves  impose  an  extra  strain.  Heart-block, 
auricular  flutter  and  auricular  fibrillation,  nodal  rhythm,  and 
even  extra-systoles,  are  all  injurious.  The  effects  are  well 
seen  in  parox3^smal  tachycardia,  in  which  the  heart  dilates 
and  the  hver  swells  and  oedema  makes  its  appearance  in 
the  extremities,  if  the  paroxysm  lasts  longer  than  a  few^^ 
hours. 

Extrinsic  factors  may  come  into  action.  They  are  innumer- 
able and  may  act  in  various  ways.  The  records  of  athletics 
contain  many  examples  of  a  heart  strained  by  severe  physical 
exertion,  and  even  death  may  result,  as  in  the  recent  Marathon 
race  at  Stockholm.  Failure  is  more  likely  to  occur  in  a  heart 
whose  reserve  is  lessened  b}^  chronic  valvular  disease,  and  the 
exertion  need  not  be  great  or  long-continued.  In  cases  of  high 
blood-pressure,  the  pressure  usualh^  rises  as  years  pass,  and 
the  extra  strain  one  day  becomes  too  great  for  the  muscle  to 
overtake. 

The  strain  may  fall  upon  the  right  ventricle  instead  of  the 
left,  from  some  affection  of  the  lungs,  bronchitis,  pneumonia^ 
or  the  Hke;  and  the  strain  may  be  progressive,  if  progressive 
emphysema  ensues.  The  right  heart,  it  must  be  remembered, 
is  already  overworked  in  mitral  disease  and  in  affections  of  the 
pulmonary  and  tricuspid  valves.  . 

Symptoms  may  succeed  a  gastro-intestinal  upset  ^dth  its 
accompanying  disturbance  of  nutrition  and  its  varied  intoxi- 
cations ;  an  operation ;  a  mental  shock ;  or  starvation  in  any 
form.     An  acute  exacerbation  of  chronic  renal  mischief  is  fre^^ 
quently  the  last  straw. 

In  another  group  symptoms  ensue  as  a  result  of  the  cardiac 
disease,  but  yet  indirectly.     An  embolus  may  be  set  free  from  a 


286  DISEASES  OF  THE  HEART 

clot  in  the  auricles  or  on  a  valve,  and  a  coronary  artery  may  be 
blocked,  or  an  infarct  of  the  lungs  or  a  cerebral  softening  may 
take  place,  and  cardiac  failure  follow. 

The  most  frequent  symptom  in  chronic  valvular  disease  is 
shortness  of  breath,  of  which  the  majority  of  patients  make  more 
or  less  complaint.  It  may  be  frequency  of  respiration  (poly- 
pncea)  or  difficulty  in  breathing  (dyspnoea),  or  associated  with 
distress  when  lying  dowTi,  so  that  the  patient  is  forced  to  main- 
tain the  upright  position  (orthopnoea).  Cheyne-Stokes  or 
cyclic  breathing  maj'  occur.  The  distress  may  only  be  felt  on 
exertion,  or  may  obtain  during  rest  as  well;  and  not  infre- 
quently is  most  marked  during  the  night. 

'  Shortness  of  breath  occurs  in  many  diseases.  It  may  be  due 
to  anaemia  or  to  disease  of  the  lungs  ;  it  may  be  associated  with 
abdominal  conditions,  such  as  the  enlarged  uterus  of  late  preg- 
nancy, which  mechanically  interfere  with  the  free  movements 
of  the  diaphragm;  or  may  be  the  result  of  toxaemia.  Com- 
parable causes  may  be  active  in  cardiac  disease.  Some  patients 
are  notably  anaemic.  The  weakness  of  the  left  heart  may  be 
so  great  that  systemic  ischaemia  ensues  even  on  trivial  exertion. 
The  lungs  are  often  more  or  less  engorged  and  pulmonary 
oedema  is  the  rule,  if  the  failure  is  well  marked ;  bronchitis  and 
emphysema  often  co-exist ;  and  an  infarct  or  pleural  effusion 
may  add  to  the  respiratory  difficulties.  An  enlarged  liver 
or  ascites  may  hinder  the  movements  of  the  diaphragm.  Asso- 
ciated renal  or  hepatic  disease  may  produce  toxaemia. 
\^  It  is  important  to  recognize  in  each  individual  case  the  par- 
^  ticular  factor  that  is  in  action,  and  this  is  usually  easy  if  a 
routine  examination  is  made,  for  the  signs  of  bronchitis,  pul- 
monary oedema,  ascites,  etc.,  are  distinctive.  Toxic  causes 
may  occasion  difficulty,  for  chronic  renal  disease  of  the  cirrhotic 
type  is  not  invariably  accompanied  by  albuminuria;  which, 
conversel}",  may  be  merely  the  result  of  chronic  venous  conges- 
tion. The  blood-pressure  is  here  a  useful  guide,  for  it  is  not 
elevated  in  simple  valvular  disease,  save  in  cases  of  aortic 
regurgitation,  so  that  a  high  blood-pressure  indicates  the 
existence  of  some  extra-cardiac  comphcation,  such  as  arterial 
or  renal  disease,  and  so,  most  frequently,  defective  ehmination. 


FlU.    140. — BuiCIItAL  AND   KE31'L 


'URVES  IN  GhEVNE-StOKES    IJRBiTniNa,    SdOWING   VARIATIONS  IN  THl:;   PeILSE-RATE. 

The  two  uurvus,  however,  do  uot  cuiacido. 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     287 

The  character  of  the  respiratory  distress,  too,  is  important,  for 
paroxysmal  dyspnoea  is  always  toxic  in  origin ;  while  orthopncea, 
in  the  absence  of  gross  pulmonary  or  abdominal  mischief,  owns 
a  similar  cause. 

In  the  typical  form  of  Cheyne-8tokes  breathing  periods  of 
apnoea  and  dyspnoea  alternate.  The  respirations,  at  first  weak 
and  infrequent,  gradually  become  deeper  and  more  numerous, 
and  then  gradually  wane  until  respiration  wholly  ceases.  The 
alternation  is  sometimes  incomplete,  and  no  real  apnoea  occurs, 
though  periods  of  weak  infrequent  breathing  alternate  with 
periods  during  which  it  is  full  and  frequent.  Similar  variations 
may  occur  in  the  pulse-rate,  which  is  generally  more  rapid 
during  apnoea,  but  the  respiratory  and  pulse  variations  do  not 
coincide  exactly,  though  they  exhibit  similar  curves  (Fig.  146); 
and  the  relationship  may  be  reversed,  so  that  the  pulse-rate  is 
more  frequent  during  dyspnoea;  it  is  often  unchanged.  A 
"  pulsus  alternans  "  may  occur  during  dyspnoea,  if  the  respira- 
tions number  half  the  pulse-rate  (Fig.  97);  the  smaller  beat 
occurs  at  the  maximum  of  inspiration. 

The  periods  of  apnoea  vary  in  duration  and  may  last  for  a 
second  or  two,  or  for  nearly  half  a  minute  or  even  longer.  If 
the  period  is  long,  the  patient  often  becomes  unconscious 
and  may  close  his  eyes  and  cease  talking,  individual  muscles 
may  twitch,  and,  rarelj^,  general  convulsions  occur.  In  the 
lesser  degrees  the  intelligence  may  be  unimpaired.  If  the  eye- 
lids remain  open,  the  size  of  the  pupils  may  be  seen  to  vary ;  they 
usually  contract  during  apnoea,  and  dilate  during  dyspnoea ; 
but  the  phenomenon  is  inconstant  and  variable. 

Cheyne-Stokes  breathing  is  most  frequently  noticed  at  night, 
though  it  may  be  continuous ;  and  in  many  cases  the  patient  is 
greatly  distressed,  for  as  soon  as  he  goes  to  sleep  the  period- 
icity is  exaggerated  and  apnoea  prolonged,  and  at  the  end  of 
each  period  he  wakens  up  in  distress,  covered  with  profuse 
perspiration,  and  may  have  to  sit  up  in  bed  to  recover  his 
breath.  In  the  lesser  grades  symptoms  maj^  be  absent.  In 
some  cases  the  breathing  is  periodic  or  cycHc,  the  waxing  and 
waning  of  the  typical  Cheyne-Stokes  paroxysm  being  absent, 
the  patient  merely  ceasing  to  breathe  for  a  few  seconds  at  more 
or  less  irregular  intervals. 


288  DISEASES  OF  THE  HEART 

Paroxysmal  attacks  of  breathlessness  occasionally  occur. 
They  are  most  common  at  night,  the  patient  as  a  rule  suddenly 
awakening  from  sleep  in  an  access  of  intense  dyspnoea,  which 
necessitates  his  sitting  bolt  upright  in  bed.  Expiration  is 
prolonged,  and  the  chest  is  full  of  rhonchi.  After  an  interval 
of  some  duration  (minutes  to  hours),  relief  is  obtained,  but 
some  orthopnoea  generally  persists.  The  attacks  tend  to  recur, 
and  the  distress  may  be  so  great  that  the  patients  are  afraid  to 
go  to  sleep, 

A  cough  and  spit  are  not  uncommon.  The  cough  is  usually 
accompanied  by  spit,  and  due  to  a  slight  catarrh,  or  oedema  of 
the  lungs  ;  but  it  is  sometimes  an  isolated  symptom  and  may  be 
extremely  troublesome.  The  sputum  may  be  of  varied  kind; 
mucoid  or  muco-purulent  from  catarrh;  watery  and  perhaps 
copious  in  oedema  of  the  lungs,  when  a  spittoonful  or  more  may 
be  expectorated  in  twenty -four  hours  ;  or  haemorrhagic .  Haemop- 
tysis in  chronic  mitral  disease  is  verj^  seldom  due  to  pulmonary 
phthisis.  In  mitral  stenosis  it  occasionally  occurs  from  capil- 
lary rupture  when  the  congestion  of  the  vessels  is  extreme; 
aud  several  ounces  may  be  voided.  As  a  rule  it  ceases  quickly, 
though  it  may  recur,  and  the  patient  is  conscious  of  improve- 
ment in  his  general  condition.  In  one  of  my  patients,  a  girl 
who  had  been  sent  to  a  sanatorium  from  an  error  in  diagnosis, 
the  relief  was  so  distinct  that  she  welcomed  the  recurrence  of  the 
haemorrhage.  In  the  other  valvular  lesions  simple  rupture  is 
unusual,  and  the  most  common  cause  of  blood  in  the  sputum 
is  a  pulmonary  infarct.  The  bleeding  in  this  case  is  not  accom- 
panied by  relief,  but  rather  by  an  exaggeration  of  the  symp- 
toms, and  the  breathlessness  may  be  suddenly  intensified  and 
accompanied  by  pain  in  the  side  from  associated  pleurisy.  The 
physical  signs  of  a  consolidation  are  usually  apparent  on  ex- 
amination. The  prognosis  is  always  serious,  for  a  pulmonary 
infarct  is  evidence  as  a  rule  of  gross  stasis  in  the  right  auricle, 
and  is  thus  the  accompaniment  of  a  considerable  failure  of 
compensation,  and  is  hkely  to  occur  towards  the  end  of  the 
iUness ;  but  in  exceptional  cases  a  fair  recovery  may  ensue  and 
persist. 

Cough  without  spit  is  by  no  means  common.     Sir  William 
Osier  has  reported  some  cases  of  mitral  stenosis  with  laryngeal 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     289 

palsy,  in  which  the  recurrent  laryngeal  nerve  was  pressed  upon 
by  the  dilated  right  auricle ;  in  some  cough  was  persistent. 

Cardiac  discomfort  or  pain  is  frequently  experienced.  The 
most  common  complaint  is  of  palpitation,  the  patient  becoming 
conscious  of  the  cardiac  contractions  as  a  fluttering  or  throbbing 
sensation  within  the  chest. 

Palpitation,  of  course,  obtains  in  healthy  individuals  under 
the  stress  of  severe  physical  exertion  or  deep  emotion;  and  is 
not  unusual  in  other  persons  whose  cardiac  work  is  carried  on 
easily  and  well;  its  most  common  cause  is  gastric  flatulence. 
But  its  occurrence  without  obvious  cause  is  always  a  matter  of 
importance,  and  calls  for  a  detailed  examination  of  the  heart. 
In  cardiac  disease  it  may  be  due  to  several  causes.  It  occurs 
on  slight  exertion  in  cases  where  the  cardiac  work  is  being 
carried  on  with  difficulty.  The  disability  is  generally  apparent 
in  other  ways  as  well,  and  a  mild  degree  of  cyanosis  or  oedema, 
an  enlarged  and  tender  liver,  or  a  frequent  pulse-rate,  are 
obvious  on  examination.  Palpitation  of  this  kind  is  most 
common  in  patients  with  large  hearts,  in  particular  those  asso- 
ciated with  renal  disease,  arterio-sclerosis,  and  aortic  regurgita- 
tion. In  the  latter  case  the  arterial  pulsations  may  be  very 
forcible  and  the  patient's  head  may  shake  visibly  with  each 
pulsation ;  and  I  have  even  felt  the  bedstead  on  which  a  pn  tient 
was  lying  shake  with  each  beat  of  the  heart. 

In  other  cases  palpitation  occurs  even  when  the  patient  is  at 
rest,  and  is  then  most  often  due  to  a  disturbance  of  the  normal 
rhythm  of  the  heart.  The  occurrence  of  an  extra-systole  may 
thus  be  apparent,  the  individual  being  conscious  either  of  the 
long  pause — the  intermission — or  of  the  strong  post-extra- 
systolic  contraction.  More  rarely  the  extra-systole  itseK  is 
felt.  But  in  many  cases,  particularly  if  extra-systoles  are 
frequent,  or  if  the  post-extra-systolic  pause  is  short,  the  patient 
may  be  unaware  of  the  irregularity.  Palpitation  is  usual  in 
auricular  flutter,  auricular  fibrillation,  nodal  rhythm,  and 
heart-block,  the  irregularity  in  the  force  of  the  ventricular 
contractions  in  the  second,  and  the  shock  of  the  auricular  con- 
traction when  the  auriculo- ventricular  values  are  shut  in  the 
others,  being  perceptible.     The  palpitation  of  the  tachycardia 

19 


290  DISEASES  OF  THE  HEART 

of  exophthalmic  goitre  maj"  be  due  to  a  similar  cause ;  for  when 
the  pulse  is  very  frequent,  ventricular  diastole  is  of  short  dura- 
tion, and  auricular  contraction  may  ensue  before  the  preceding 
ventricular  systole  is  ended. 

Palpitation  is  most  common  when  the  cardiac  action  is  fre- 
quent, and  is  comparatively  rare  when  the  pulse-rate  is  below 
normal.  In  full  heart-block,  however,  occasional  beats  may 
be  felt,  presumably  when  auricle  and  ventricle  happen  to  con- 
tract simultaneously. 

/  Pain  may  be  occasioned  in  several  ways  and  may  be  referred 
to  various  situations.  Epigastric  pain  of  a  dull,  aching  char- 
acter, intensified  by  pressure  and  often  by  the  ingestion  of 
food,  is  usually  associated  with  a  large  congested  liver,  which 
can  easily  be  felt  upon  palpation ;  and  somewhat  rarely  may  be 
due  to  cholecystitis,  which  occurred  in  a  patient  who  was 
recently  under  my  care  for  severe  cardiac  failure.  Embolism 
often  occasions  abdominal  pain,  which  may  be  very  severe. 
The  most  common  cause  is  embolism  of  the  spleen,  in  which 
case  the  pain  is  generally  referred  to  the  left  side,  and  friction 
may  be  audible  on  auscultation;  but  the  pain  may  be  general. 
A  woman,  aged  forty-six,  who  had  suffered  from  symptoms  of 
mild  cardiac  failure  for  a  couple  of  years,  was  one  day  seized, 
without  obvious  cause,  with  griping  abdominal  pain,  which 
was  so  severe  that  she  fell  down  upon  the  floor  and  was  unable 
to  move  until  her  husband  came  home  from  work  five  hours  later 
and  lifted  her  into  bed.  The  only  obvious  cause  on  'post-mortem 
examination  was  a  splenic  infarct.  In  another  patient  who 
was  already  in  hospital,  abdominal  pain  of  severe  character 
suddenly  ensued  when  he  was  lying  quietly  in  bed,  and  re- 
quired the  administration  of  morphia ;  the  stools  on  the  next 
day  contained  blood  in  large  amount.  Post-mortem  examina- 
tion revealed  a  blocked  mesenteric  artery  with  necrosis  of 
several  feet  of  the  small  bowel,  and  general  peritonitis. 

Thoracic  pain  also  owns  several  causes.  It  may  be  due  to 
pulmonary  infarct  and  pleurisy,  and  is  then  usually  referred  to 
the  side  of  the  chest.^  It  may  be  due  to  pericarditis,  and  is  then- 
prsecordial  in  site.  It  may  be  paroxysmal  and  of  anginous 
type,  preecordial  in  site,  but  often  spreading  to  the  head  and 
arms.     A  clear   distinction   should   be   drawn   between   con- 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE    291 

tinuous  and  paroxysmal  pain,  for  the  former  is  almost  always 
associated  with  a  gross  visceral  lesion,  while  the  latter  may  be 
due  to  functional  disturbance. 

The  degree  of  thoracic  discomfort  varies  considerably  in 
different  patients.  In  some  the  complaint  is  frequent,  but  the 
distress  is  probably  trivial,  and  no  objective  evidence  of  cardiac 
weakness  may  be  apparent.  A  choking  sensation,  a  short  bout 
of  palpitation,  or  a  sense  of  constriction  round  the  chest,  may 
thus  be  called  pain  by  some  individuals,  while  in  others  Httle 
reference  is  made  to  discomfort,  and  complaint  is  made  of  pain 
alone. 

Cardiac  cedema  contrasts  with  that  of  renal  disease  in  being 
most  marked  in  the  lower  extremities,  and  first  noticed  in  the 
evening,  if  the  patient  has  been  walking  about  during  the  day ; 
and  minimal  in  the  morning,  after  he  has  been  lying  flat  in  bed. 
(Edema  may  be  considerable  without  attracting  the  attention 
of  the  patient.  The  rapid  variations  in  the  weight  of  cardiac 
patients  from  time  to  time  is  generally  due  to  fluctuations  in 
the  amount  of  fluid  in  the  subcutaneous  tissue,  and  a  stone's 
weight  may  be  present  without  any  very  obvious  signs.  In 
patients  who  are  confined  to  bed,  the  sacrum  and  the  back  of 
the  thighs  may  be  oedematous,  if  they  are  the  most  dependent 
parts,  though  the  shins  scarcely  pit. 

The  oedema  spreads  upwards  and  may  involve  the  scrotum 
and  the  serous  sacs.  Q^]dema  of  the  prepuce  may  interfere 
with  micturition,  but  the  difficulty  can  always  be  temporarily 
overcome  by  firm  pressure  on  the  foreskin  with  the  fingers. 
Pleural  effusions,  on  the  right  side  more  frequently  than  on  the 
left,  are  perhaps  more  common  than  ascites,  but  ascites  may  be 
missed  if  the  patient  is  orthopnoeic,  for  the  pelvis  can  contain 
a  considerable  quantity  of  fluid  without  any  obvious  signs  of 
its  presence.  Pleural  effusion  may  occasion  considerable 
respiratory  distress  even  when  the  amount  is  small. 

In  a  general  way  the  oedema  and  effusions  steadily  increase 
from  below  upwards,  and  any  deviation  from  the  rule  indicates 
the  activity  of  some  new  factor.  Pleural  adhesion,  for  instance, 
may  prevent  pleural  transudation,  and  should  be  suspected, 
if  one  pleural  cavity  is  full  and  the  other  empty;  and  thepres- 


294  DISEASES  OF  THE  HEART 

lution,  may  all  occur.  Many  patients  complain  of  constant 
throbbing  in  the  head ;  this  is  most  frequently  associated  with 
aortic  regurgitation.  Headache  and  insomnia  are  often  accom- 
panied by  paroxysmal  dyspnoea  or  by  orthopnoea,  and  are 
usually  due  to  toxaemia  and  associated  with  a  high  blood- 
pressure.  Mental  symptoms  may  obtain;  cases  with  nocturnal 
dyspnoea  often  suffer  from  disturbing  dreams,  which  may 
appear  as  real  occurrences  during  their  waking  hours ;  or  may 
be  mildly  dehrious  or  stupid.  Acute  mania  is  rare;  dementia 
is  not  uncommon,  but  is  most  usually  associated  with  evidence 
of  organic  cerebral  disease. 

The  Symptoms  of  Mitral  Disease. — It  is  impossible  to  draw 
a  sharp  chnical  distinction  between  mitral  stenosis  and  mitral 
regurgitation.  Their  causes  are  similar — acute  endocarditis 
in  early  life  and  chronic  endocarditis  in  later  years — and  both 
are  frequently  associated  with  chronic  arterial  and  renal 
disease.  Regurgitation,  however,  owns  one  cause  which  is 
pecuhar  to  itself.  The  orifice  of  the  mitral  valve  is  large, 
while  the  cusps  are  relatively  smaU  and  quite  incapable  of 
closing  the  aperture  unless  it  is  narrowed  by  the  contraction 
of  the  sphincter  muscle.  In  anaemia  and  in  debility  from  any 
cause,  this  sphincter  action  may  fail, and  a  temporary  "func- 
tional "  mitral  reflux  ensue.  A  comparable  reflux  may  also  occur 
in  cases  of  aortic  valvular  disease  or  high  blood-pressure,  where 
a  special  strain  is  thrown  upon  the  left  ventricle.  The  presys- 
toUc  murmur  is  always  a  sign  of  organic  valvular  disease,  but  the 
systoHc  murmur  may  be  due  to  a  temporary  and  curable  cause. 

In  the  majority  of  cases  of  organic  valvular  disease  stenosis 
and  incompetence  co-exist,  though  the  degree  of  each  varies  in 
individual  cases,  the  stenosis  being  sometimes  considerable 
and  sometimes  trivial;  and  vice  versa.  In  many  cases  a  double 
murmur  is  present,  but  in  others  one  alone  persists,  and  an 
accurate  diagnosis  may  be  impossible  during  life.  Thus,  in 
auricular  fibrillation,  the  characteristic  crescendo  murmur  dis- 
appears mth  the  cessation  of  co-ordinate  auricular  contrac- 
tion ;  and  it  also  fails  when,  as  in  nodal  rhythm  and  heart-block, 
the  auricular  contractions  do  not  regularly  precede  the  ven- 
tricular contractions.  The  presystohc  murmur,  too,  may 
alone  obtain  in  cases  where   post-mortem  the  mitral  orifice  is 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     295 

found  to  be  patent,  and  the  cusps  so  stiff  and  hard  that  it 
seems  impossible  that  it  could  ever  have  been  closed.  Re- 
gurgitation in  these  cases  is  prevented  by  the  high  blood- 
pressure  within  the  auricle,  which  is  raised  by  the  contraction 
of  the  right  ventricle  to  such  a  height  that  blood  can  only  flow 
slowly,  if  at  all,  from  left  ventricle  to  left  auricle  during  ven- 
tricular systole,  and  too  slowly  to  produce  an  audible  murmur. 
The  presystolic  murmur  is  the  one  that  most  often  disappears, 
and  my  own  experience  agrees  with  that  of  Graham  Steell,* 
who  states  that  "  the  murmur  most  frequently  present  in 
cases  of  mitral  stenosis  is  unquestionably  the  murmur  of 
coincident  incompetence." 

In  both  lesions  the  pulmonary  blood-pressure  is  high.  In 
stenosis  the  elevation  is  continuous,  for  the  obstruction  at  the 
mitral  valve  necessarily  remains  constant.  In  regurgitation, 
on  the  other  hand,  the  elevation  is  intermittent,  for  though, 
when  the  ventricles  are  in  systole,  the  left  auricle  is  distended 
by  blood  flowing  into  it  from  the  left  ventricle  and  the  pul- 
monary veins,  the  congestion  is  rapidly  relieved  when  diastole 
succeeds,  as  no  obstacle  is  now  presented  to  the  free  flow  of 
blood  into  the  left  ventricle ;  and  the  auricular  blood-pressure 
in  consequence  rapidly  falLs.  Dilatation  of  the  left  auricle  is 
for  this  reason  as  a  rule  more  extreme  in  cases  of  stenosis,  and 
clots  in  the  auricular  appendages  are  more  common,  and  em- 
bolic phenomena  more  frequent. 

In  mitral  incompetence  the  left  ventricle  is  dilated  and  hyper- 
trophied.  During  ventricular  systole  the  left  auricle  is  dis- 
tended by  blood  flowing  into  it  from  the  left  ventricle  and  the 
pulmonary  veins,  and  the  left  ventricle,  in  consequence,  receives 
during  diastole  a  larger  amount  of  blood  than  normal.  The 
larger  complement,  too,  is  necessary  if  compensation  is  to  be 
sufficient,  for  a  normal  amount  of  blood  in  the  left  ventricle 
would  be  insufficient  to  supply  the  aorta  with  its  proper  amount, 
if  some  of  the  blood  regurgitated  at  the  same  time  into  the 
left  auricle.  Mitral  stenosis,  on  the  other  hand,  has  no  effect 
upon  the  left  ventricle,  but  only  on  the  left  auricle  and  the 
right  ventricle ;  and  left  ventricular  hypertrophy,  when  it  obtains, 
is  due  to  other  causes,  aortic  valvular,  arterial,  or  renal  disease. 
*  "  Diseases  of  the  Heart,"  Manchester,  1906. 


296  DISEASES  OF  THE  HEART 

The  onset  of  symptoms  may  be  gradual  or  abrupt.  The 
slighter  s^^mptoms  are  often  insidious,  but  those  which  bring 
the  patient  under  observation  as  a  rule  ensue  more  or  less 
suddenly.  Thus  in  MacDonald's  series  the  onset  was  gradual 
in  36  cases,  and  more  or  less  sudden  in  66. 

In  the  exceptional  case  the  symptoms  may  arise  with 
dramatic  abruptness,  A  woman,  aged  forty-three,  had  ex- 
perienced shght  breathlessness  and  palpitation  on  exertion  for 
some  years,  but  of  so  trivial  a  degree  that  she  paid  no  attention 
to  the  discomfort  and  sought  no  advice.  One  morning  her 
husband,  on  awakening,  discovered  that  she  was  unable  to 
speak  and  could  not  move  the  right  arm  or  leg.  On  post- 
mortem  examination  a  large  cortical  softening  was  found  in 
the  left  cerebral  hemisphere,  and  weU-marked  mitral  stenosis. 
The  embolus  was  evidently  derived  from  clots  in  the  left 
auricle.  Such  a  course  of  events  is,  however,  uncommon,  but 
serious  symptoms  may  arise  within  a  few  days.  A  man,  aged 
forty-six,  a  foreman  with  a  firm  of  horse-dealers,  took  a  ship- 
load of  horses  to  Canada  for  sale.  On  September  21  he  ran 
the  horses  in  the  show-yard  without  discomfort.  He  imme- 
diately sailed  for  home,  but  on  the  voyage  bad  weather  was 
encountered,  and  on  the  27th  his  cabin  was  flooded.  Bron- 
chitis ensued,  and  two  days  later  his  legs  were  cedematous. 
On  admission  to  hospital  the  cardiac  failure  was  extreme,  but 
he  made  a  good  recovery.  The  bronchitis  had  overtaxed  a 
right  heart  already  strained  by  a  double  mitral  lesion.  A 
woman,  aged  thirty-five,  who  had  always  been  healthy  save 
for  an  attack  of  acute  rheumatism  at  the  age  of  twenty, 
noticed  that  her  feet  were  swollen  after  the  sixth  month  of  her 
fourth  pregnancy.  Labour  was  difficult  and  prolonged,  and 
chloroform  was  administered;  she  lost  a  considerable  quantity 
of  blood.  The  oedema  rapidly  disappeared,  and  she  felt  quite 
well  when  she  rose  from  bed  on  the  ninth  day  after  dehvery, 
but  it  returned  within  a  week,  and  steadily  increased  in 
amount,  and  she  became  Yevy  short  of  breath,  even  while  at 
rest.  The  failure  continued,  and  she  died  some  months  after- 
wards. The  strain  of  pregnancy  and  a  post-haemorrhagic 
anaemia  had  occasioned  the  failure  of  compensation. 

The  onset  may  be  gradual.     A  httle  wizened  old    woman 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     297 

enters  my  wards  every  few  montiis  suffering  from  extreme 
general  weakness  and  considerable  oedema.  She  has  a  well- 
marked  presystolic  murmur.  Improvement  is  always  rapid, 
and  in  a  month  or  six  weeks  she  has  gained  a  stone  in  weight 
and  feels  in  excellent  health.  But  she  drinks  heavily,  and  after 
a  few  weeks  invariably  loses  her  employment  and  is  half 
starved ;  and  the  symptoms  slowly  recur. 

The  onset  of  symptoms  may  be  determined  by  various 
causes.  Twenty-two  of  MacDonald's  cases  were  admitted  to 
hospital  on  account  of  other  diseases  (acute  rheumatism, 
II;  influenza  (?),  6;  scarlatina,  gonococcic  arthritis,  pleurisy, 
gastritis,  ruptured  pyloric  ulcer,  1).  In  13  cases  symptoms 
foUowed  exposure  to  cold  and  chill,  and  in  10  cases  child- 
birth, and  in  2  more  arose  during  pregnancy ;  in  5  they  suc- 
ceeded exertion  (a  "  flitting,"  a  game  of  football,  a  dance). 
Starvation,  angina  pectoris,  the  shock  of  a  husband's  iUness 
and  death,  the  extraction  of  several  teeth,  etc.,  are  included 
in  his  list. 

The  Symptoms  o!  Aortic  Disease. — In  aortic,  as  in  mitral 
disease,  it  is  impossible  to  draw  a  sharp  distinction  between 
stenosis  and  incompetence,  for  the  two  lesions  frequently  co- 
exist, though  the  degree  of  each  varies  in  individual  cases. 
In  a  general  way  incompetence  is  much  more  common  than 
stenosis,  and  the  more  serious  fault;  but,  whenever  the  cusps 
are  stiffened,  their  mobihty  is  lessened  and  the  orifice  is  shghtly 
narrowed,  and  double  murmurs  are,  in  consequence,  audible; 
even  trivial  vegetations,  too,  may  produce  a  systohc  murmur. 

The  diastohc  murmur  is  almost  always  a  sign  of  organic 
disease  of  the  valves,  or  at  am'  rate  of  permanent  incom- 
petence, for  though  it  may  occur  without  any  lesions  of  the  cusps 
from  dilatation  of  the  aortic  orifice,  the  connective  and  elastic 
tissues  of  the  wall,  when  once  stretched,  never  regain  their 
former  condition. 

These  cases  are  uncommon,  but  my  colleague.  Dr.  George  S. 
Middleton,  recently  showed  me  a  specimen  from  a  patient 
who  had  died  in  his  wards .  The  valve  was  grossly  incompetent 
to  the  water-test,  but  the  cusps  were  only  shghtly  thickened 
and  were  not  retracted,  though  they  were  quite  incapable  of 
closing  the  greatly  dilated  orifice.     The  ascending  aorta,  too, 


298  DISEASES  OF  THE  HEART 

was  dilated,  the  walls  being  affected  by  an  advanced  syphilitic 
aortitis . 

In  a  few  rare  cases,  however,  the  murmur  may  be  incon- 
stant, and  this  may  occur  both  in  acute  endocarditis  and  in 
chronic  degenerative  lesions .  In  the  former  case  large  vegeta- 
tions may  temporarily  stop  the  leak;  in  the  latter  the  leak 
may  be  minimal  for  a  time.  The  loudness  of  a  murmur 
depends  upon  two  factors — the  rapidity  of  the  blood-current 
and  the  nature  of  the  valvular  fault;  and  may  vary  from 
variations  in  the  first  factor,  though  the  second  remains  con- 
stant. An  old  man  who  was  attending  my  out-patient  clinique 
had  at  one  time  a  diastolic  murmur  which  was  only  audible 
immediately  after  exertion;  it  disappeared  after  ten  minutes' 
rest.  In  the  course  of  some  months  the  murmur  was  con- 
stantly present,  and  as  the  other  symptoms  increased  he  was 
admitted  into  hospital  and  put  to  bed.  Two  days  later  the 
murmur  was  absent  so  long  as  he  was  in  the  recumbent  position, 
though  it  reappeared  whenever  he  stood  erect. 

With  physical  exercise  the  blood-pressure  rises,  and  the 
difference  between  the  blood-pressures  within  the  aorta  and  the 
left  ventricle  during  ventricular  diastole  is,  in  consequence, 
increased.  The  backward  flow  may  now  be  sufficiently  rapid  to 
produce  an  audible  murmur,  though  during  rest  the  pressures 
approximate,  the  rate  of  flow  lessens,  and  the  murmur  dis- 
appears. In  this  patient,  as  the  incompetence  progressed, 
the  murmur  became  audible  whenever  gravity  was  in  action 
and  the  difference  in  pressure  was  augmented,  though  it  was 
absent  when  the  patient  was  recumbent. 

An  inconstant  murmur  as  a  rule  in  time  becomes  constant, 
but  a  few  cases  have  been  recorded  in  which  the  murmur  has 
never  returned.  The  explanation  is  difficult  to  understand. 
In  a  still  more  rare  group  the  diastolic  murmur  may  be  absent, 
though  post-mortem  the  valve  is  stenosed,  and  the  cusps  so 
stiff  and  hard  that  it  seems  certain  that  the  orifice  was  always 
open,  while  to  the  water-test  it  is  markedly  incompetent. 

The  normal  blood-pressure  within  the  aorta  is  considerable 
(100  to  130  mm.  Hg),  while  the  aortic  cusps  are  thin  and 
fragile,  and  it  has  been  suggested  that  they  are  of  themselves 
insufficient  to  prevent  leakage,  unless  supported  on  the  ven- 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     299 

tricular  side  by  the  apposition  of  the  subjacent  muscle.  If 
the  aortic  bulb  is  dilated,  the  support  fails,  and  regurgitation 
ensues.  With  recovery  the  muscular  pads  resume  their 
function,  and  the  leak  is  stayed ;  while,  conversely,  in  valvular 
disease  the  muscular  mechanism  may  be  sufficient  to  prevent - 
regurgitation.  Keith  considers  that  though  the  subaortic 
musculature  does  contract  and  narrow  the  lumen  during  the 
systole  of  the  ventricles,  its  contraction  ceases  during  diastole, 
and  that  it  can  have  little  if  any  effect  in  preventing  regurgita- 
tion at  this  period  of  the  cardiac  cycle.  Stewart,  however, 
maintains  that  the  musculature  of  the  aortic  conus  enters  into 
contraction  later  than  the  rest  of  the  ventricular  muscle,  and 
remains  contracted  during  the  early  part  of  diastole,  thus 
affording  the  aortic  cusps  efficient  support  until  the  intra- 
ventricular pressure  rises,  with  the  influx  of  blood  from  the  left 
auricle,  to  such  a  height  that  regurgitation  can  only  be  minimal. 
The  systoMc  aortic  murmur,  on  the  other  hand,  is  by  no  means 
definite  evidence  of  aortic  stenosis.  It  is  often  present  when 
the  cusps  are  merely  hard  and  stiff  or  coated  with  small  vegeta- 
tions in  such  trivial  degree  that  little  obstruction  can  obtain, 
and  frequently  occurs  in  anaemia  or  debihty,  and  disappears  as 
soon  as  the  general  condition  is  improved.  In  fact,  as  an 
isolated  sign,  it  is  more  frequently  associated  with  a  normal 
than  with  an  abnormal  valve. 

The  effects  of  aortic  valvular  disease  are  at  first  confined  to 
the  systemic  circulation  and  to  [the  left  ventricle.  In  stenosis 
the  lesion  hinders  the  entrance  of  blood  into  the  aorta  and 
tends  to  produce  systemic  anaemia ;  in  incompetence  the  blood 
enters  the  aorta  readily  during  systole,  but  re-enters  the  ven- 
tricle as  soon  as  diastole  succeeds ;  the  systemic  anaemia  is 
intermittent.  In  stenosis  the  lesion  tends  to  lower  the  blood- 
pressure,  though,  as  a  matter  of  fact,  it  is  generally  high  from 
associated  arterial  and  renal  disease.  In  incompetence  the 
blood-pressure  is  necessarily  elevated  as  a  result  of  the  in- 
competence ;  for  if  the  mean  blood-pressure  within  the  aorta 
is  to  be  maintained,  the  initial  pressure  must  be  above  the 
normal  to  compensate  the  rapid  fall  which  occurs  during  the 
early  part  of  diastole.     The  variations  in  pressure  may  be 


300 


DISEASES  OF  THE  HEART 


large  if  the  leak  is  great,  and  the  pulse-pressure  (the  difference 
between  the  systolic  and  diastolic  pressures)  is  an  accurate 
index  of  the  degree  of  the  mechanical  fault  (Fig.  147).  Some  of 
the  symptoms — the  throbbing  in  the  head,  palpitation,  etc.- — are 
the  result  of  this  sudden  variation  of  the  arterial  blood-pressure. 


'******, 


'  O  <9  rvx  >v,  . 


Fig.  147. — Blood-Pressuke  Chart:  Aortic  Regurgitation. 

The  pulse  pressure  (55  mm.)  exceeds  the  diastolic  pressure.     Note  the  large  shotty 

pulse. 

Aortic  stenosis  is  compensated  by  ventricular  hypertrophy, 
but  in  incompetence  the  ventricle  must  be  larger  than  normal 
as  well  as  hypertrophied ;  for  if  the  normal  amount  of  blood  is 
to  be  left  in  the  arteries  at  the  end  of  diastole,  the  amount 
thrown  into  them  during  systole  must  be  greater  than  normal 
to  compensate  the  loss  which  occurs  during  diastole.  In  aortic 
reflux  the  left  ventricle  may  be  very  large. 


SYMPTOMS  OP  CHRONIC  VALVULAR  DISEASE     301 

The  strain  of  aortic  lesions  is  thus  thrown  primarily  upon 
the  left  ventricle,  and  as  long  as  it  is  able  to  do  its  work,  symp- 
toms are  in  abeyance.  But  if  the  work  required  is  more  than 
it  can  undertake,  it  dilates  under  the  strain,  the  sphincter 
muscle  of  the  mitral  valve  fails  to  close  the  orifice,  mitral 
reflux  occurs,  and  the  symptoms  of  an  engorged  pulmonary 
circulation  are  superadded  to  those  of  the  original  lesion.  In 
the  majority  of  aortic  cases  the  onset  of  serious  symptoms  is 
synchronous  with  the  onset  of  mitral  reflux,  and  in  great 
measure  its  result,  and  aortic  and  mitral  disease  thus  produce 
symptoms  of  the  same  type,  though  they  vary  in  their  incidence 
and  in  their  degree.  In  mitral  disease  symptoms  ensue  when 
the  right  heart  fails ;  in  aortic  disease  when  the  left  heart  fails. 

Aortic  disease  is  associated  with  arterial  and  renal  lesions 
with  even  greater  frequency  than  is  the  case  in  mitral  disease, 
and  the  symptoms  which  obtain  are  often  only  partly  due  to 
the  cardiac  element.  Their  onset  may  be  gradual  or  sudden, 
but  is  most  often  the  former,  being  sudden  in  only  15  of 
MacDonald's  series  of  58  cases.  In  some  cases  they  suc- 
ceed some  physical  exertion,  as  was  the  case  with  a  man, 
aged  fifty-three,  in  active  business,  whose  aortic  valves  were 
known  to  have  been  incompetent  for  two  years,  though  no 
evidence  of  cardiac  weakness  had  been  shown,  and  who  had  a 
serious  faint  as  the  initial  symptom  after  a  hard  day's  work  in 
hot  weather.  In  another  case,  an  engineer  aged  twenty-five, 
whose  valvular  disease  had  been  recognized  for  several  years 
but  had  not  interfered  with  his  occupation,  hemiplegia  suddenly 
ensued  when  he  was  running  to  overtake  an  uncle  whom  he 
saw  walking  in  front  of  him.  Sometimes  the  symptoms  follow 
a  pulmonary  catarrh,  as  was  the  case  with  a  man,  aged  forty- 
seven,  who  became  notably  breathless  during  an  influenzal 
attack,  though  the  evidence  of  pulmonary  disturbance  was 
trivial.  And  sometimes  they  arise  without  evident  cause.  A 
man,  aged  sixty,  who  had  not  been  looking  well  for  some 
months  according  to  his  medical  attendant,  whom,  however, 
he  had  not  consulted,  took  a  hot  bath  one  night  at  10  p.m. 
At  midnight,  when  lying  quietly  in  bed  reading,  he  suddenly 
became  extremely  breathless  and  had  to  sit  up  in  bed.  The 
dyspnoea  passed  off  in  ten  minutes,  but  from  that  time  he  was 


302  DISEASES  OF  THE  HEART 

always  conscious  of  his  heart's  action  as  a  constant  throbbing 
within  the  chest. 

The  early  symptoms,  when  the  onset  is  insidious,  are  also 
often  associated  with  physical  exertion.  A  man,  aged  forty- 
six,  for  instance,  who  was  accustomed  to  hard  physical  exercise, 
admitted  that  he  had  been  getting  more  short-winded  than  he 
used  to  be  for  a  year  before  the  symptoms  really  troubled  him. 

Symptoms  may,  of  course,  occur  without  obvious  cause.  A 
farmer's  wife,  aged  sixty,  who  had  always  been  healthy  and 
active,  save  for  an  attack  of  scarlatina  at  the  age  of  twenty, 
and  blood-poisoning  from  a  prick  of  the  finger  at  forty-four, 
noticed  in  the  spring  of  1909  that  her  feet  were  often  swollen 
at  night,  and  that  she  became  short  of  breath  on  trivial  exer- 
tion; but  she  was  able  to  continue  her  work  notwithstanding 
her  discomforts.  In  the  spring  of  1910  the  symptoms  became 
exaggerated,  and  she  was  forced  to  take  to  bed  and  to  seek 
medical  advice.  The  aortic  lesion  was  progressive,  and  the 
symptoms,  in  consequence,  became  more  serious. 

The  onset  of  symptoms  may  be  due  to  various  causes, 
but  is  most  frequentty  insidious  (43  out  of  58  cases).  In 
MacDonald's  series  5  patients  ascribed  their  illness  to  ex- 
posure and  chill;  5  were  admitted  suffering  from  acute 
rheumatism;  2  were  suffering  from  notable  distress  in 
breathing,  which  had  ensued  suddenly  when  they  were  at 
work;  3  were  admitted  unconscious,  1  after  an  epileptic  fit, 
and  1  hemiplegic.  The  modes  of  onset  thus  contrast  with 
those  of  mitral  disease,  a  fact  which  is  to  be  related  to  the 
difference  in  the  incidence  of  their  various  causes.  In  aortic 
cases  these  causes  are  as  a  rule  progressive  in  their  nature, 
while  from  the  proximity  of  the  coronary  arteries  to  the  valve 
these  vessels  are  extremely  apt  to  be  abnormal,  and  the 
nutrition  of  the  cardiac  muscle  suffers  in  consequence.  A 
rheumatic  scar  on  a  mitral  valve  may  cease  to  contract,  and 
rarely  affects  the  coronary  arteries. 

The  Symptoms  o5  Mitral  and  Aortic  Disease. — The  symptoms 
of  mitral  disease  are  most  often  respiratory,  and  ninety-one  of 
MacDonald's  series  complained  more  or  less  of  breathlessness. 
In  mitral  disease  the  pulmonary  circulation  is  always  con- 
gested, and  the  normal  respiratory  activity  is  impeded ;  mitral 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     303 

patients  are  often  cyanosed.  Bronchitis  is  a  frequent  com- 
plication, and  occurred  in  39  cases.  It  may,  as  already  men- 
tioned, originate  sj-mptoms,  and  in  their  presence  always 
intensijQes  the  distress.  One  of  my  chronic  hospital  patients 
with  mitral  disease  and  auricular  fibrillation  was  quite  com- 
fortable and  able  to  do  light  work  so  long  as  his  chest  was  clear, 
but  had  serious  cardiac  failure  whenever  he  contracted  a  cold 
in  the  chest. 

Pulmonary  infarct  and  haemoptysis  are  common  in  mitral 
disease,  and  occurred  in  18  cases.  Twenty  patients  were 
orthopnceic;  in  10  the  breathing  was  difficult;  in  3  the 
dyspnoea  was  spasmodic  and  paroxysmal.  Orthopnoea  is 
generally  accompanied  by  abdominal  distension  (due  to  flatu- 
lence or  ascites)  or  by  an  enlarged  Hver.  The  upright  position 
relieves  the  pressure  upon  the  diaphragm  and  permits  a  greater 
excursion.  Dyspnoea  is  frequently  associated  with  auricular 
fibrillation,  which  was  present  in  19  cases.  It  may  of  course 
be  due  to  other  causes,  but  the  sterno-mastoid  muscles 
are  almost  always  habitually  in  action  whenever  the  pulse  is 
permanently  irregular. 

In  aortic  disease  shortness  of  breath  is  also  the  most  common 
symptom,  and  was  present  in  54  cases  of  MacDonald's 
series.  It  is  not,  however,  related  so  closely  to  passive  venous 
congestion  of  the  lungs  as  in  mitral  disease,  for  this  is  minimal 
or  absent  unless  the  ventricle  dilates  and  the  mitral  valve 
becomes  incompetent.  Puhnonary  embohsm  is  unusual,  and 
did  not  occur  in  this  series,  so  that  death  seems  to  occur  before 
any  considerable  strain  is  thrown  upon  the  right  heart.  Short- 
ness of  breath  is  frequently  due  to  bronchitis,  which  was 
present  in  greater  or  less  degree  in  37  cases ;  and  may  also 
result  from  systemic  ischsemia,  being  then  experienced  on 
exertion.  This  result  is  more  hkely  to  foUow  if,  as  is  often 
the  case,  the  patient  is  anaemic.  The  degree  of  anaemia 
is  rarely  considerable,  but  in  one  case  the  red  ceUs  only 
numbered  2,000,000,  with  a  haemoglobin  value  of  35  per  cent. 
Auricular  fibrillation  is  uncommon,  and  was  only  present  in 
two  cases. 

In  aortic  cases  shortness  of  breath  is  not  unusual  when  the 
patient  is  at  rest   (20  cases),    and  is   often  worse  at  night. 


304  DISEASES  OF  THE  HEART 

Nine  patients  were  orthopnoeic,  and  11  had  difficulty  in 
breathing ;  in  6  of  these  the  dyspnoea  was  spasmodic  and 
paroxj^smal.  The  majority  of  the  patients  were  over  forty 
years  of  age  (over  forty,  33;  under  forty,  25),  and  the  prob- 
abihty  of  a  toxic  origin  is,  in  consequence,  considerable.  The 
question  is  difficult  to  answer,  but  10  of  the  13  cases  examined 
post-mortem  showed  some  form  of  nephritis ;  and  of  the  6 
patients  in  whom  the  dyspnoea  was  paroxysmal  2  had  granular 
kidnej^s,  while  all  the  others  had  persistent,  though  shght, 
albuminuria. 

Forty-nine  of  the  mitral  patients  complained  of  palpitation, 
and  30  suffered  from  thoracic  pain.  In  one  case  typical 
attacks  of  angina  occurred.  The  distinction  between  dis- 
comfort and  actual  pain  is  sometimes  difficult  to  establish, 
for  the  descriptions  of  the  patients  vary  according  to  their 
sensitiveness,  and  are  often  evidently  inaccurate.  A  woman, 
aged  twentj'-seven,  who  was  suffering  from  a  double  mitral 
lesion,  became  one  morning  quite  suddenly  very  short  of  breath. 
The  respirations  were  more  frequent  than  they  had  been,  and 
the  pulse  had  doubled  in  rate  and  was  running  about  160. 
At  intervals  paroxysms  of  intense  dyspnoea  ensued,  during  which 
her  distress  became  intensified;  the  attacks  lasted  for  about 
fifteen  minutes.  She  said  that  she  had  no  actual  pain,  but 
that  her  discomfort  was  unbearable,  though  she  had  described 
her  previous  attacks  as  "painful."  Paroxysmal  tachycardia, 
then,  occasions  discomfort,  and  so  may  auricular  fibrillation 
and  extra-systoles.  Pericarditis  is  probabty  a  more  common 
cause  than  is  realized,  for  a  local  pericarditis  is  not  uncommonly 
found  on  fost-7nortem  examination,  which  had  given  rise  to  no 
evident  signs  during  Mfe.  A  girl  who  was  suffering  from  an 
acute  endocarditis  complained  of  pain  in  the  upper  part  of  her 
chest  for  a  few  hours  on  December  29.  On  February  11  the 
pain  recurred  during  the  night,  again  lasting  for  a  short  time. 
On  March  3  she  had  severe  pain  over  the  heart  for  twenty -four 
hours,  and  on  March  5  pericardial  friction  was  audible.  It 
seemed  probable  that  pericarditis  was  the  cause  of  the  recurring 
attacks,  but  that  the  inflammation  was  local,  and  subsided  on 
the  two  first  occasions.  In  another  patient  thoracic  pain  was 
due  to  arthritis  of  the  sterno-clavicular  joints,  apparently  of 


SYIIPTOMS  OF  CHRONIC  VALVULAR  DISEASE     305 

rheumatic  origin  and  associated  with  large  crops  of  subcu- 
taneous nodules. 

Epigastric  pain  was  present  in  15  cases.  In  many  more  the 
liver  was  tender  on  palpation. 

Nineteen  of  the  aortic  cases  complained  of  palpitation,  and 
22  of  thoracic  pain,  which  in  17  cases  was  preecordial  in  site. 
One  patient  suffered  from  typical  anginous  attacks,  and  4  ex- 
perienced a  sense  of  constriction  around  the  chest.  Thoracic 
discomfort  is  thus  almost  equally  common  in  mitral  and  aortic 
disease,  but  palpitation  is  less,  and  pain  is  more,  frequent  in 
the  aortic  group.  The  frequency  with  which  auricular  j&brilla- 
tion  occurs  in  mitral  disease  (19  of  102  mitral  cases;  2  of  58 
aortic  cases)  explains  the  more  common  complaint  of  palpita- 
tion in  this  group,  while  the  predominance  of  pain  in  the  aortic 
cases  must  be  ascribed  to  the  frequency  of  associated  arterial 
disease  involving  the  aorta  and  the  coronary  arteries .  Aneurism 
occurred  in  9  of  the  aortic  and  in  2  of  the  mitral  cases. 
Epigastric  pain,  on  the  other  hand,  is  unusual,  and  was  only 
present  in  2  instances.  _-^ 

(Edema  was  present  in  51  of  MacDonald's  mitral  cases,  and 
was  considerable,  and  invaded  the  trunk  in  22.  In  some  it 
was  trivial  and  subsided  rapidty  as  soon  as  the  patient  Avas 
-confined  to  bed,  but  in  others  it  was  extreme,  and  in  1  case 
the  skin  of  the  legs  gave  way  and  the  fluid  drained  through 
the  apertures.  The  four  causes  of  oedema — cardiac  failure, 
renal  disease,  anaemia,  and  obstruction  of  veins — may  all  be 
active  in  a  cardiac  case.  ,The  first  three  are  often  present; 
the  last  is  unusual.  Oile  of  vd.y  patients,  however,  complained 
of  pain  in  her  right  calf,  which  was  tender  to  palpation ;  the 
overlying  skin  became  red  and  glazed.  The  discomfort  sub- 
sided in  a  couple  of  days,  but  a  fortnight  later  the  left  leg 
became  oedematous,  and  the  femoral  vein  was  tender  and 
cord-hke.  A  pulmonary  infarct  occurred,  but  she  made  a  good 
recovery.  Renal  oedema  is  universal,  while  cardiac  oedema 
is  distributed  in  accordance  with  the  law  of  gravity.  The 
scalp  frequently  pits  on  pressure  in  renal  disease,  but  I  have 
never  found  this  to  occur  in  cases  of  cardiac  failure  where  the 
Sidneys  seem  to  be  normal.     Local  oedema  owns  a  local  cause.- 

In  aortic  disease  oedema  is  slightlj-  less  frequent,  and  is  rarely 

20 


306  DISEASES  OF  THE  HEART 

considerable.     It  was  present  in  24  patients,  but  was  only 
considerable  in  5. 

In  exceptional  cases,  however,  it  may  be  both  persistent 
and  extreme,  and  in  one  old  lady,  aged  sixty,  who  was  admitted 
into  my  wards  it  was  present  for  twenty-one  months,  for  ten 
of  which  she  was,  in  consequence,  confined  to  bed.  On  her 
admission  the  oedema  was  extreme,  and  practically  universal, 
and  involved  the  serous  sacs  to  such  a  degree  that  paracentesis 
was  required.  The  mitral  valve,  however,  was  incompetent 
as  well  as  the  aortic,  and  the  right  heart  was  notably  dilated. 

Gastric  symptoms  are  frequently  present  in  mitral  disease. 
Twenty-two  patients  complained  of  anorexia,  34  of  vomiting, 
12  of  varjdng  gastric  discomfort.  One  patient  suffered  from 
acute  gastritis. 

In  aortic  disease,  on  the  other  hand,  gastric  symptoms  are 
uncommon.  Six  patients  complained  of  anorexia,  and  4  of 
gastro-intestinal  discomfort. 

-/  Embolic  phenomena  are  not  uncommon  in  mitral  disease. 
A  married  woman,  aged  forty-six,  had  suffered  for  some  year& 
from  shortness  of  breath  and  palpitation  on  exertion,  but  was 
able  to  do  her  household  duties  without  distress .  Two  months 
before  admission  she  ran  a  short  distance  to  catch  a  tramcar, 
and,  on  arriving  beside  it,  was  so  weak  that  she  was  unable  to 
get  into  it.  She  felt  very  breathless  and  faint,  but  after 
leaning  against  a  wall  for  ten  minutes  was  sufficiently  recovered 
to  walk,  with  her  son's  assistance,  the  few  hundred  yards  to 
her  house.  She  had  great  difficulty  in  ascending  the  stairs, 
and  had  to  take  a  rest  on  several  occasions.  Next  day  she  felt 
much  better,  and  got  up  for  a  few  hours,  and  within  a  week 
was  doing  her  usual  work.  Two  weeks  later,  when  alone  in 
her  house,  she  suddenly,  without  obvious  reason,  experienced 
a  griping  pain  in  the  abdomen,  which  was  so  severe  that  she 
fell  to  the  floor,  where  she  lay  for  five  hours,  until  her  husband 
returned  and  assisted  her  to  bed.  The  pain  persisted  for  a 
day  or  two,  but  gradually  lessened,  though  slight  attacks 
recurred  from  time  to  time.  The  palpitation  became  more 
troublesome,  and  continued  even  when  she  was  at  rest.  On 
the  day  before  admission,  when  she  was  sitting  in  a  chair,  she 
suddenly  felt  extremely  weak,  and  vomited,  but  the  discomfort 


SYMPTOMS  OF  CHRONIC  VALVULAR  DISEASE     307 

ceased  within  ten  minutes.  On  admission  to  hospital,  on 
February  15,  she  was  seen  to  be  fairly  well  developed  but 
poorly  nourished,  and  white  hair  made  her  look  older  than  her 
years.  She  lay  easily  in  bed,  and  there  was  no  csdema,  but 
the  liver  was  enlarged  and  tender,  rhonchi  were  audible  all 
over  the  chest,  and  the  pulse  was  frequent  and  extremely 
irregular  (auricular  fibrillation).  Both  sides  of  the  heart  were 
enlarged.  No  murmurs  were  audible,  but  the  first  sound  at 
the  apex  was  short  and  sharp,  with  an  abrupt  commencement, 
and  the  second  pulmonic  sound  was  emphatic.  The  urine 
contained  blood  and  albumin  in  amount,  and  numerous  tube- 
casts.  Some  improvement  occurred  within  the  next  few  days, 
but  on  the  evening  of  February  28  she  experienced  pain  in  her 
right  leg,  which  prevented  her  from  sleeping ;  it  had  disappeared 
next  day,  and  nothing  abnormal  could  be  seen.  On  March  19 
she  complained  bitterly  of  numbness  in  the  left  leg  and  foot, 
but  again  examination  was  negative.  On  the  evening  of 
April  6  she  suddenly  fell  back  unconscious,  her  breathing 
becoming  stertorous,  and  a  left  facial  palsy  was  apparent. 
In  a  few  hours  consciousness  returned.  She  had  a  restless 
night,  but  next  morning  spoke  clearly  and  intelligibly ;  a  shght 
paresis  was  evident  on  the  left  side,  but  she  could  move 
her  limbs.  On  April  15  she  suddenly  lost  consciousness  for 
ten  minutes,  but  rapidly  recovered.  On  April  20  she  com- 
plained of  pain  in  the  right  side  of  the  abdomen,  and  felt  sick 
and  vomited.  Cyanosis  became  extreme,  but  the  symptoms 
subsided  in  a  couple  of  days .  The  pain  and  vomiting  recurred 
on  May  14,  and  lasted  again  for  two  days ;  but  on  May  18  she 
suddenly  lost  consciousness  and  passed  into  coma,  dying  a  few 
hours  later. 

On  'post-inortem  examination  many  infarcts  were  found,  a 
small  one  in  the  lower  lobe  of  the  right  lung,  four  in  the  spleen, 
and  five  in  the  kidneys.  In  the  brain  there  was  a  white  cica- 
tricial area  above  and  behind  the  posterior  end  of  the  right 
internal  capsule,  and  a  haemorrhagic  infarct  of  more  recent 
origin  in  the  pons ;  the  right  middle  cerebral  artery  was  oc- 
cluded by  an  embolus  near  its  origin ;  the  cerebral  vessels  were 
not  diseased.  The  mitral  valve  was  the  site  of  an  extreme 
button-hole  stenosis ;  the  left  auricle  was  greatly  enlarged  and 


308  DISEASES  OF  THE  HEART 

its  walls  hypertrophied.  The  auricular  appendix  was  particu- 
larly large,  and  completely  fiUed  by  an  enormous  tough  throm- 
bus, which  measured  some  3  inches  in  length,  and  projected  as  a 
polypoid  mass  into  the  cavity  of  the  auricle.  The  free  surface 
was  in  parts  coated  with  soft  recent  clot. 

The  cause  of  the  various  symptoms  was  thus  apparent.  The 
abdominal  pain  was  due  to  splenic  infarcts,  the  pain  on  the 
right  side  to  the  pulmonary  infarct,  and  the  hsematuria,  in 
part  at  any  rate,  to  the  renal  ones.  The  cerebral  symptoms 
owned  a  similar  cause. 

Embohc  phenomena  are  unusual  in  aortic  disease.  None 
occurred  in  this  series. 

Cerebral  sj^mptoms  are  more  common  in  aortic  than  in  mitral 
disease.  Of  the  mitral  patients,  4  suffered  from  hemiplegia, 
18  complained  of  headache,  9  of  giddiness,  8  of  faintness,  and 
1  of  noises  in  the  head.  In  the  aortic  group  2  suffered  from 
hemiplegia,  7  complained  of  headache,  9  of  giddiness.  3  of 
faintness,  6  of  insomnia,  and  2  of  a  sensation  of  impending 
death. 

The  exact  cause  of  these  symptoms  may  be  diificult  to 
determine  during  hfe.  Two  of  the  mitral  hemiplegias  were 
due  to  embohsm,  and  one  to  haemorrhage.  One  of  the  aortic 
hemiplegias  had  a  cerebral  haemorrhage.  No  post-mortem 
examination  w^as  made  in  the  other  cases.  The  headache 
sometimes  suggests  a  definite  cerebral  lesion,  but  is  most 
often  associated  wdth  high  blood-pressure  and  evidence  of 
renal  disease;  sometimes  it  seems  to  be  due  to  anaemia.  Gid- 
diness is  most  frequent  in  patients  with  degenerate  arteries, 
while  faintness  is  not  necessarity  associated  wdth  anaemia  or 
extreme  cardiac  weakness .  In  one  of  my  patients  who  fainted 
frequently,  as  a  rule  after  exertion,  the  only  other  sign  of 
cardiac  disabihty  w'as  very  slight  oedema  of  the  shins.  In 
some  patients  "  faints  "  are  probably  petit  mal. 

Of  general  sjrmptoms  the  most  frequent  is  weakness,  which 
was  present  in  33  mitral  cases  and  in  13  aortic  patients.  Three 
mitral  patients  complained  of  coldness  of  the  extremities  and 
1  of  epistaxis.  One  aortic  patient  made  complaint  of  failing 
eyesight. 


CHAPTER  XXIII 
MYOCARDIAL  FAILURE  WITHOUT  VALVULAR  DISEASE 

In  chronic  valvular  disease  th.e  cardiac  work  maj^  be  carried 
on  for  many  years  without  any  signs  of  cardiac  distress,  symp- 
toms only  making  their  appearance  when  the  muscle  becomes 
unable  to  accompKsh  its  necessary  task.  The  failure  may  be 
due  to  many  causes ;  the  occurrence  of  a  new  factor,  such  as 
bronchitis,  throwing  an  extra  strain  upon  the  heart ;  an  in- 
crease in  the  grade  of  the  valvular  disturbance  to  such  a  point 
that  the  reserve  is  overwhelmed ;  or  the  appearance  of  patho- 
logical changes  in  the  muscle  itself. 

Myocardial  disease  may,  however,  occur  in  the  absence  of 
valvular  lesions,  and  may  produce  very  evident  symptoms  of 
cardiac  distress ;  but  though  the  chnical  picture  may  be  purely 
cardiac,  pathological  investigation  shows  that  the  lesions  are 
rarely,  if  ever,  confined  to  the  heart.  The  granular  degenera- 
tion of  the  acute  infections  is  accompanied  by  cloudy  swelling 
in  other  viscera ;  fatty  degeneration  of  the  heart  is  associated 
with  fatty  degeneration  elsewhere;  fatty  infiltration  usually 
affects  the  whole  body,  and  not  the  heart  alone;  while  the 
arterial  lesions  of  fibrosis  are  rarely  hmited  to  the  coronary 
arteries . 

The  symptoms  of  myocardial  weakness  are  similar  to  those 
which  occur  in  valvular  disease  when  compensation  has  broken 
down. 

In  the  infections  the  symptoms  of  cardiac  failure  are  obscured 
by  those  of  the  toxaemia  and  those  produced  by  any  local  lesions 
which  may  be  present ;  but  the  increasing  weakness,  breathless- 
ness,  and  cyanosis,  which  are  so  commonly  present  in  serious 

309 


310  DISEASES  OF  THE  HEART 

cases,  are  due,  ir  part  at  any  rate,  to  cardiac  weakness.  Cold- 
ness, pallor,  or  congestion  of  the  extremities,  are  by  no  means 
infrequent,  and  faintness  or  intense  prostration  may  occur 
even  on  trivial  exertion,  such  as  sitting  up  in  bed.  (Edema 
during  the  progress  of  an  acute  infection  is  of  somewhat  rare 
occurrence,  and  is  most  often  the  result  of  venous  thrombosis ; 
but  it  may  be  purely  cardiac,  and  though  usually  trivial,  is 
occasionally  widespread  and  extreme. 

A  married  woman,  aged  thirty,  who  had  nursed  her  fourth 
baby  for  nine  months,  gradually  began  to  find  that  her  house- 
work was  becoming  exhausting,  and  that  she  became  short  of 
breath,  and  felt  her  heart  beating  on  very  slight  exertion. 
Vomiting  set  in,  and  continued  for  several  weeks .  She  lost  flesh 
rapidly,  and  became  pale  and  sallow  in  appearance.  On  admis- 
sion to  hospital,  she  was  very  weak  and  exhausted,  and  notably 
emaciated  and  pale,  the  red  cells  only  numbering  1,060,000, 
with  a  haemoglobin  value  of  20  per  cent.  Films  showed  a  well- 
marked  megalocytic  reaction.  A  few  days  afterwards  she 
became  fevered,  and  a  consolidation  gradually  involved  the 
left  lung.  With  the  onset  of  the  pneumonia  exhaustion  be- 
came extreme  and  incontinence  ensued,  and  coincident ly 
oedema,  which  on  admission  had  been  trivial  in  amount,  became 
universal  and  considerable.  The  pulse  was  now  very  small 
and  soft  and  frequent,  and  the  cardiac  sounds  were  short  and 
weak.  Three  weeks  later  the  consolidation  was  resolving,  the 
oedema  had  disappeared,  and  the  pulse,  though  still  small  and 
soft,  approximated  to  the  normal  rate.  She  eventual^  made 
a  good  recovery,  and  four  years  later  was  strong  and  well. 

During  convalescence  from  the  infections,  on  the  other  hand, 
the  usual  symptoms  of  cardiac  weakness,  shortness  of  breath 
on  exertion,  and  oedema,  are  extremely  common,  and  are  some- 
times very  persistent,  though  in  the  vast  majority  of  cases  they 
disappear  rapidly  with  improvement  of  the  general  liealth. 
Cardiac  discomfort,  palpitation,  tachycardia,  and  pain  may 
also  occur,  and  may  suggest  from  their  continuance  the  possi- 
bihty  of  serious  mischief,  though  complete  recovery  is  the  rule, 
unless  organic  disease  is  abeady  present.  The  palpitation  and 
tachycardia  are  extremely  trying  to  the  patient,  and  may  con- 
tinue for  months.     In  the  case  of  a  medical  friend,  after  an 


MYOCARDIAL  FAILURE  311 

influenza]  attack,  even  such  trivial  exertion  as  walking  slowly 
upstairs  induced  profuse  perspiration,  with  throbbing  of  the 
Avhole  chest  and  head,  while  the  pulse-rate  ran  up  to  the 
neighbourhood  of  200  per  minute.  A  sensation  of  faintness  is 
common,  but  actual  syncope  is  rare. 

Fatty  Changes. — 'The  fatty  changes  which  occur  in  the  heart 
are  as  a  rule  associated  with  disease  elsewhere,  and  give  but 
little  clinical  evidence  of  a  specific  kind.  Fatty  degeneration 
is  most  common  in  severe  anaemia,  in  chronic  alcohohsm,  in 
emphysema,  and  in  chronic  disease  of  the  kidneys,  and  the 
cardiac  symptoms  are  only  a  part  of  a  general  disturbance.  It 
co-exists  with  granular  changes  in  the  infections,  but  its  particu- 
lar degree  cannot  be  appreciated  during  life;  and  in  disease  of 
the  coronar}" 'arteries  it  is  only  a  phase  of  an  ischsemic  atrophy. 
So  that,  as  an  isolated  lesion  affecting  the  heart  and  the  heart 
alone,  it  is  of  rare  occurrence,  although  cardiac  weakness  from 
fatty  changes  frequentl}^  occurs. 

Fatty  infiltration  is  as  a  rule  merely  a  part  of  a  general  ten- 
dency to  obesity,  whose  presence  naturally  suggests  the  nature 
of  any  existing  myocardial  weakness.  But  with  obesitj',  again, 
renal  and  arterial  disease  are  frequently  combined,  and  the 
cardiac  picture  is,  in  consequence,  obscured. 

It  seems  probable  that  there  is  no  real  distinction  between 
fatty  infiltration  and  fatty  degeneration,  which  differ  in  site 
rather  than  in  nature.  The  quality  of  the  fat  has  been  shown 
to  be  the  same  in  the  two  situations  in  animals  in  which  the  lesion 
has  been  produced  experimentally,  and  fats  which  are  abnormal 
to  the  species  may  be  deposited,  if  a  particular  fatty  dietary  is 
adopted.  Fatty  infiltration,  too,  is  invariably  accompanied 
by  a  certain  amount  of  fatty  degeneration,  though  the  converse 
proposition  is  by  no  means  universally  true. 

In  the  exceptional  case  fatty  infiltration  of  the  muscle  occiu-s 
without  the  epicarclial  or  the  general  fat  being  excessive.  The 
causes  of  this  are  not  yet  recognized;  but  the  fact  is  of  im- 
portance, as  the  nature  of  the  cardiac  weakness  is  apt  to  be  mis- 
interpreted. A  striking  example  of  this  once  came  under  my 
observation.  An  old  man  who  was  convalescing  apparently 
satisfactorih'  from  a  mild  attack  of  smallpox,  somewhat  sud- 
denly became  weak  and  stupid,  and  passed  rapidly  into  semi- 


312  DISEASES  OF  THE  HEART 

coma  and  into  coma,  dying  within  forty-eight  hours  of  the 
onset  of  serious  symptoms.  There  had  been  no  symptoms 
previously  which  suggested  anj'  special  cardiac  weakness,  and 
his  general  nutrition  seemed  good,  and  there  was  no  special 
obesity-.  The  heart,  however,  shoAved  extreme  fatty  infiltra- 
tion, particularly  upon  the  right  side,  where  fatty  deposits  were 
visible  even  on  the  endocardial  surface;  and  the  muscle  cells 
were  also  grossly  affected.  His  arteries  generally  were  athero- 
matous and  hard,  and  the  minute  arterioles  on  the  right  side  of 
the  heart  were  affected  to  a  greater  degree  than  on  the  left. 

The  symptoms  of  fatt}^  change  in  the  heart  do  not  differ  from 
those  of  cardiac  weakness  owning  other  causes,  and  the  evi- 
dences of  cardiac  insufficiency  are  similar.  The  heart,  too,, 
from  associated  lesions  may  be  large  or  small;  the  pulse  may 
be  hard  and  full,  or  small  and  soft ;  and  the  murmurs  indicative 
of  valvular  disease,  or  alterations  of  the  sounds  from  high 
blood-pressure  or  a  hardened  aorta  may  be  absent  or  present 
in  particular  instances.  The  thickness  of  the  parietal  fat  in 
general  obesity  may  interfere  with  the  examination  of  the 
heart,  and  the  character  of  the  pulse  may  be  the  sole  trust- 
worthj'  guide.  One  is  not  infrequently  scarcely  able  to  hear 
the  cardiac  sounds,  though  the  pulse  is  full  and  hard,  with  a 
pressure  decidedly  above  the  normal. 

Disease  of  the  Coronary  Arteries. — The  relative  frequency 
with  which  individual  arteries  are  diseased  has  been  investi- 
gated b}^  several  writers.  Everyone  is  agreed  that  the  aorta 
is  most  frequently  affected,  but  while  Lobstein  states  that  the 
splenic  and  the  femoral  arteries  are  more  often  diseased  than 
the  coronary  arteries,  and  Rokitansky  gives  precedence  as  well 
to  the  iliac  vessels,  Huchard  considers  that  the  arteries  of  the 
heart  are  those  which  are  most  frequently  abnormal.  For  this 
predominance  several  reasons,  he  states,  are  apparent.  Their 
high  origin  in  the  aorta,  where  the  blood-pressure  is  at  a  maxi- 
mum, their  mainly  muscular  texture,  their  numerous  and 
acute  curves,  their  constant  activity  in  supplying  blood  to 
tissues  constantly  in  action,  etc.,  all  tend  to  render  them  unduly 
liable  to  disease;  while  their  relationship,  however  well  pro- 
tected they  may  be  in  their  bed  of  fat  in  the  sulci,  to  the  regu- 


MYOCARDIAL  FAILURE  313 

larly  contracting  heart,  exposes  them  constantly  to  jars  and 
contusions.  The  exact  reason  for  their  affection,  however,  is 
of  less  moment  than  its  frequency,  and  the  importance  of  their 
integrity  cannot  be  over-estimated,  for  upon  their  integrity  the 
nutrition  of  the  heart  depends. 

Myocardial  disease  is  rarely,  if  ever,  universal,  and  the  local 
distribution  is  dependent  upon  local  and  most  commonly  vas- 
cular causes ;  and,  as  we  have  seen,  atrophy,  fatty,  and  hyaline 
degeneration,  necrosis  and  fibrosis,  may  aU  be  due  to  arterial 
disease.  In  arterio-sclerosis  the  arterial  change  is  widespread, 
and  the  coronary  lesions  can  be  appreciated  by  recognition 
of  the  existence  of  the  change  in  the  peripheral  vessels ;  but  in 
focal  disease  the  distribution  is  often  erratic  and  apparently 
whimsical,  and  the  visceral  vessels  may  be  seriously  affected 
Avithout  any  evident  change  in  the  arteries  which  are  accessible 
to  examination.  It  is  this  factor  which  makes  prognosis  in 
cardiac  disease  so  imperfect,  for  our  ignorance  of  the  condition 
of  the  coronary  arteries  renders  it  impossible  to  assess  the  most 
important  factor  at  its  true  value,  and  the  "  happy  guess  " 
sometimes  turns  out  to  be  wrong.  An  embolus  occludes  the 
lumen,  a  narrowed  vessel  becomes  completely  blocked,  and  the 
cardiac  contractions  suddenly  and  for  ever  cease. 

Occlusion  of  the  coronary  arteries  may  be  of  gradual  or  of 
sudden  onset,  and  may  affect  the  superficial  "rings  "  or  the 
perforating  branches.  The  anastomotic  connections  of  the 
rings  may  prevent  any  serious  damage  to  the  muscle  if  the 
occlusion  is  sufficiently  gradual,  and  several  cases  in  which  this 
occurred  have  been  already  considered.  But  rapid  closure 
prevents  adequate  compensatory  arrangements,  and  the 
muscle  which  is  concerned  in  consequence  dies.  Even  in 
gradual  closure  adequate  anastomotic  developments  are  excep- 
tional, and  the  muscle  suffers  in  greater  or  less  degree.  Closure 
of  a  nutrient  end-artery  always  produces  necrosis. 

The  changes  which  are  found  post-mortem  may  thus  vary 
from  variations  in  the  rapidity  of  the  closure  and  in  the  site 
of  the  affected  vessel.  And  while  at  one  end  of  the  chain, 
where  the  anastomotic  developments  are  sufficient,  the  cardiac 
muscle  may  be  perfectly  normal,  and  at  the  other,  where  a  large 
vessel  has  been  suddenly  closed,  it  may  show  no  microscopic 


314  DISEASES  OF  THE  HEART 

lesions,  because  sudden  death  has  prevented  structural  changes, 
the  intervening  hnks  exhibit  every  intervening  grade  in  extent 
and  severity,  and  the  clinical  symptoms  follow  suit.  Death 
may  ensue  in  a  moment,  or  after  an  illness  of  many  months, 
and  serious  failure  may  pass  away  if  satisfactory  anastomotic 
developments  eventually  follow. 

Experimental  ligation  of  a  coronary  artery  or  of  one  of  the 
main  branches  is  often  rapidly  followed  by  death,  but  this  is 
by  no  means  invariable,  and  the  animals  may  live  for  hours, 
days,  or  even  weeks  without  the  appearance  of  any  notable 
symptoms  beyond  a  transient  irregularity  of  the  cardiac  action ; 
and  a  case  has  been  recorded  (Pagenstecker,  quoted  by  Hirsch- 
f elder)  in  which  the  right  coronary  artery  of  a  man  was  liga- 
tured without  harm.  Clinical  and  pathological  observations 
show  similar  results,  and  the  changes  which  are  found  even  in 
cases  of  sudden  death  often  show  that  coronary  occlusion  must 
have  occurred  some  time  previously. 

If  the  occlusion  is  sudden  and  complete,  immediate  death 
may  ensue.  A  woman,  aged  thirty-two,  underwent  a  some- 
what tedious  operation  for  gall-stones,  and  on  the  next  morning 
was  very  cheery  and  well,  but  about  noon  died  suddenly,  and 
without  any  warning.  On  examination,  a  large  mobile  embolus 
was  found  to  block  completely  the  descending  branch  of  the 
left  coronary  artery,  which  was  otherwise  normal.  The  embolus 
had  arisen  from  a  clot  at  the  apex  of  the  left  ventricle,  which 
was  evidently  of  some  age,  and  must  have  existed  prior  to  the 
operation.  But  in  other  cases — e.g.,  in  rupture  of  the  heart — 
necrosis  has  occurred  previously,  and  the  fatal  issue,  though 
abrupt,  takes  place  subsequent  to  the  occlusion.  An  insane 
woman,  aged  seventy-eight,  who  went  to  bed  in  her  usual  health, 
was  found  to  be  dead  in  the  morning,  rupture  of  the  left  ventricle 
having  occurred  on  its  posterior  and  upper  aspect.  The  tissues 
at  the  site  of  rupture  were  soft  and  friable  and  necrotic,  and 
the  transverse  branch  of  the  right  coronary  artery  was  found 
to  be  thrombosed  for  nearly  an  inch.  The  inflammatory  re- 
action in  the  periphery  of  the  infarct  had  so  weakened  the 
tissues  that  the  endocardial  blood  had  gained  entrance  to  the 
muscle,  and,  forcing  its  way  along  the  track  of  the  infarct  with 
successive  contractions  of  the  heart,  ultimately  reached  and 


MYOCARDIAL  FAILURE  315 

perforated  the  pericardial  covering.  Infarcts,  too,  are  not 
necessarily  fatal,  and  may  produce  little  sign  of  cardiac  failure. 
A  woman,  aged  fifty-seven,  died  after  an  illness  of  five  days' 
duration,  during  which  the  symptoms  were  wholly  cerebral, 
the  result  of  streptococcic  abscesses  in  the  cerebellum,  and 
meningitis.  There  were  no  signs  of  special  cardiac  embarrass- 
ment, even  during  the  last  twenty-four  hours  of  life,  though 
the  mitral  valve  was  extensively  disorganized  by  recent  ulcera- 
tion superimposed  upon  a  valvular  defect  of  old  standing,  and 
a  large  infarct  was  present  at  the  apical  end  of  the  left  ventricle. 

Myocardial  Fibrosis. — In  cases  where  the  coronary  obstruc- 
tion is  gradual,  the  onset  of  symptoms  is  necessarily  insidious, 
and  the  course  of  the  disease  is  essentially  chronic — a  course 
which  is  the  rule  in  aneurism  of  the  heart ;  for  sudden  occlusion, 
if  of  any  extent,  causes  sudden  death  or  infarct,  and  in  the 
latter  case  is  more  usually  associated  with  rupture  than  with 
reparative  fibrosis. 

A  pohceman,  aged  forty-nine,  caught  cold  one  January, 
which  did  not,  however,  necessitate  his  ceasing  work;  but 
when  the  cough  had  gone  he  noticed  that  he  was  somewhat 
breathless  on  exertion,  and  experienced  a  sensation  of  tightness 
in  the  epigastric  region.  In  April  the  cough  recurred,  and  was 
now  accompanied  by  a  scanty  spit,  and  he  felt  so  unweU  that 
he  went  on  holiday  to  the  Highlands.  Here  he  improved  to 
some  extent,  but  was  still  troubled  with  breathlessness,  espe- 
cially when  walking  uphill.  On  his  return  home  he  still  felt 
unwell,  but  he  continued  at  work  until  September,  when  his 
feet  for  the  first  time  became  swollen.  At  night,  too,  he  was 
very  short  of  breath,  and  had  to  sit  up  in  bed,  and  slept  badly. 
His  weight  had  decreased,  and  he  was  2  stones  lighter  than 
usual.  On  admission  to  hospital,  the  oedema,  which  was 
general,  was  not  great,  but  the  right  chest  was  half  full  of  fluid, 
and  he  was  very  breathless  and  orthopnceic.  After  the  fluid 
had  been  removed,  his  symptoms  rapidly  abated.  The  heart 
was  large,  especially  to  the  right  side,  and  the  sounds  were 
short  and  distant,  but  pure.  The  pulse  was  regular,  but  small 
and  weak,  and  numbered  about  100,  and  even  when  his  other 
symptoms  had  disappeared  still  ran  between  90  and  100. 
After  a  month's  residence  in  hospital  he  was  sent  to  a  con- 


318  DISEASES  OF  THE  HEART 

more  or  less  abruptly  without  obvious  cause,  and  ultimately 
passes  off.  In  the  following  case  such  a  state  of  matters 
seemed  extremely  probable,  but  the  crucial  examination  is 
wanting : 

A  carter,  aged  thirty-two,  who  presented  many  of  the  signs 
of  incipient  locomotor  atax}^,  noticed  that  his  feet  had  become 
swollen  without  any  obvious  cause.  The  oedema  rapidly  in- 
creased, and  a  week  later  a  slight  cough,  accompanied  by  a 
muco-purulent  spit,  supervened,  and  the  abdomen  became 
swollen  and  tender.  When  admitted  into  hospital,  a  fortnight 
after  the  onset  of  the  iUness,  the  oedema  was  universal  and 
considerable,  the  penis  and  scrotum  being  so  much  swollen 
that  micturition  was  difficult.  The  liver  was  enlarged  and 
tender,  and  the  heart  was  large,  but  the  sounds  were  pure, 
the  first  sound  at  the  apex  being  short  and  sharp,  while  the 
second  aortic  sound  was  emphatic.  The  arteries  were  thick- 
ened and  tortuous.  Three  weeks  later  the  oedema  had  dis- 
appeared, and  the  patient's  discomforts  had  ceased,  and  his 
convalescence  was  uninterrupted.  The  failure  seemed  to  be 
purely  myocardial,  and  the  absence  of  aU  the  usual  causes  of 
failure  and  the  presence  of  widespread  arterial  disease  sug- 
gested that  it  resulted  from  disease  of  the  coronary  arteries. 
The  area  involved,  however,  was  sufficiently  sma  U  for  complete 
recovery  to  be  possible. 

The  character  of  the  sounds  in  valvular  disease  is  neces- 
sarily obscured  by  the  presence  of  murmurs,  and  the  physical 
signs  generally  may  be  grossly  altered  in  other  directions. 
The  apex  impulse  may  thus  be  displaced  b}^  associated  renal 
cirrhosis,  or  obscured  by  emphysema;  the  relative  intensity 
of  the  second  sounds  may  be  altered  by  arterial  or  by  pul- 
monary lesions ;  and  displacements  of  the  heart  may  occasion 
pulsation  in  abnormal  sites,  or  the  conduction  of  the  sounds 
in  abnormal  directions. 

It  is  often  helpful  in  these  cases  to  contrast  the  character  of 
the  apex  impulse,  the  character  of  the  pulse,  and  the  quality  of 
the  cardiac  sounds  ;  and  if  one  of  these  seems  disproportionate 
to  the  others  the  prognosis  should  be  based  on  the  more  serious 
sign.  In  renal  cirrhosis,  for  example,  the  apex  impulse  may  be 
stronger  than  normal,  and  the  pulse  of  high  pressure,  while  the 


MYOCARDIAL  FAILURE  319 

cardiac  sounds  alone  suggest  myocardial  weakness.  The  first 
sound  in  these  cases  is  rarely  sharp  or  loud,  and  is  generally 
dull  and  distant  and  faint ;  its  termination  may  be  indistinct, 
though  no  definite  murmur  is  present .  I  shall  always  remember 
the  case  of  an  old  man  dying  slowly  from  cardiac  failure  who, 
a  couple  of  days  before  his  death,  when  oedema  was  well 
marked  and  widespread,  stiU  presented  a  slow,  dehberate, 
strong  apex  impulse,  though  the  first  cardiac  sound  was  almost 
inaudible.  The  relative  intensity'  of  the  first  sound  over  the 
right  and  the  left  ventricles  should  also  be  contrasted,  for 
cardiac  strain  may  be  experienced  by  either  one  or  the  other. 
In  pneumonia  the  difference  may  be  extremely  striking,  and 
in  valvular  disease  the  sounds  in  one  or  other  situation  may  be 
pure. 


CHAPTER  XXIV 

THE  DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE 

The  diagnosis  of  the  various  valvular  affections  is  made  on 
examination  of  the  patient.  It  is  impossible  in  this  place  to 
consider  all  the  details  of  physical  examination,  but  some 
points  require  a  Kttle  special  consideration. 

The  Significance  of  Physical  Signs. — Onty  a  portion  of  the 
heart  is  directly  related  to  the  front  of  the  chest,  as  the  lungs 
overlap  all  but  a  smaU  part  of  the  right  ventricle  (Fig.  148). 
The  apex  impulse  is  thus  felt  through  a  considerable  thickness 
of  pulmonary  tissue,  and  its  character  may  be  modified  by 
variations  in  the  condition  of  the  lungs  or  pleurae,  quite  apart 
from  any  alterations  in  the  heart  itself.  It  is,  for  example, 
temporarily  weakened  on  full  inspiration  and  strengthened 
on  full  expiration,  and  it  may  be  permanently  abohshecl  by 
emphysema,  or  its  area  may  be  increased  by  retraction  of  the 
lungs.  In  health}^  individuals  it  is  freely  movable,  and  may 
be  felt  even  a  couple  of  inches  outside  its  usual  site  if  the 
individual  hes  on  his  left  side.  The  absence  of  these  physio- 
logical variations  is  important,  as  it  shows  that  the  anterior 
margin  of  the  left  lung  is  fixed,  or  that  the  apex  of  the  heart 
is  adherent  to  the  anterior  chest  wall. 

In  most  healthy  persons  the  apex  impulse  is  the  only  appre- 
ciable pulsation  on  the  front  of  the  chest.  It  is  a  definite 
forward  thrust  or  protru  'ion,  which  lasts  for  about  a  third  of 
a  second,  and  precedes  the  appearance  of  the  carotid  pulse. 
It  is  produced  by  the  cardiac  systole,  which  alters  the  shape  of 
the  heart  as  well  as  its  relation  to  the  chest  wall,  the  apex 
being  tilted  forward  and  to  the  right,  and  the  long  axis  of  the 
heart  being  slightly  lengthened;  coincidenth'  the  transverse 
diameter  of  the  heart  is  diminished.     If  the  interspaces  are 

320 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     321 


wide  and  the  chest  waU  is  thin,  a  recession  may  be  observed 
above  the  right  ventricle  between  the  apex  and  the  sternum. 

It  is  often  difficult  to  distinguish,  either  by  the  eye  or  by  the 
hand,  between  a  protrusion  and  a  recession,  for  in  both  a  for- 
ward 'movement  occurs,  though  at  different  periods  of  the 
cardiac  cycle.  (The  carotid  pulse  may  be  felt  and  the  apex 
impulse  watched.)  With  graphic  methods  the  distinction  is 
easy,  as  the  arterial  pulse  can  be  taken  as  a  guide.     Normally 


Aortic 


Tricuspid 


Puhrtonary' 


Mitral 


Fig.  148. — Diagka^i  shotting  the  StrEFACE  E.ELATIO^-s  of  Ltj:sgs,  Heaet,  and 
Cahdiac  Valves  (A.  Keith), 

the  impulse  makes   its    appearance  about  O'lO  second  before 
the  carotid,  and  0"20  second  before  the  radial  pulse. 

If  the  left  ventricle  is  hypertrophied,  the  impulse  is  wide- 
spread and  well  sustained,  and  its  relationship  to  the  arterial 
pulse  is  unchanged.  If  the  right  ventricle,  however,  is  hyper-, 
trophied,  the  apex  proper  may  be  displaced  backwards  from 
the  chest  wall,  the  impulse  which  is  felt  being  due  to  the  con- 
traction of  the  underlying  right  ventricle.     The  rhythm  of  the 

21 


322 


DISEASES  OF  THE  HEART 


impulse  is  thus  altered,  for  during  systole  the  transverse 
diameter  of  the  heart  is  lessened  and  a  recession  occurs,  the 
cardiogram  being  "inverted  "  (Fig.  150). 

In  pathological  conditions  pulsations  may  be  present  in 
various  parts  of  the  chest,  and  their  nature  can  only  be  recog- 
nized by  appreciation  of  their  character  and  rhythm.     Epigas- 


Aorta 


Pulmonary 
artery 

....  ^^/^ 

auricular 

appendix 


'Left 
ventricle 


Ri^ht  ventricle 


Fig.  149. — Diagram  showing  the  Surface  RELATioisrs  of  the  Peeicakdium, 
Heart,  and  Great  Vessels  (A.  Keith). 

trie  pulsation,  for  example,  may  be  due  to  the  pulsation  of  the 
abdominal  aorta  (Fig.  151),  to  true  hepatic  pulsation  from 
tricuspid  regurgitation,  or  to  communicated  pulsation  from 
the  heart  itself  (Fig.  153).  The  first  succeeds  the  apex  im- 
pulse, and  is  practical^  synchronous  with  the  brachial  pulse, 
and  the  others  are  synchronous  with  the  apex  impulse  and 
precede  the  brachial  pulse ;  but  if  the  pulsation  is  due  to  the 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     323 

contraction  of  the  right  ventricle  (Fig.  152)  the  tracing  is 
inverted.  The  pulsation  so  often  seen  in  the  second  left 
interspace  close  to  the  sternum  is  generally  due  to  the  pulsation 


•BTo.eK 


S'i.  Lift   SpcLCJL. 


Fig.  150. — "Inverted"  Apex  Imptjlse  (c/.  Fig.  152). 

of  the  pulmonary  artery,  as  the  main  wave  succeeds  the  apex 
impulse  and  precedes  the  brachial  pulse  (Fig.  154).  But  it 
may  be  synchronous  with  the  apex,  and  either  a  protrusion  or 


Fig.  151. — Epigastkic  Pulsation  succeeding  the  Apex  Impulse:  ABDOMiNAii 

Aorta. 

a  recession,  the  first  if  it  is  due  to  the  conus  arteriosus,  the 
second  if  it  is  due  to  contraction  of  the  right  ventricle.  The 
contraction  of  the  auricle  may  be  represented  upon  the  tracing, 


Fig    152. — Epigastric  Pulsation  synchronous  with  Apex  Impulse,  put 
inverted:  Right  Ventricle. 

usually  as  a  positive  wave,  more  rarely  inverted.  Pulsation 
to  the  right  of  the  sternum  generally  shows  an  inverted  wave, 
as  it  is  most  frequently  due  to  the  contraction  of  a  dilated  right 
heart  (Fig.  155).     But  the  wave  may  be  positive  if  it  results 


324 


DISEASES  OF  THE  HEART 


from  the  reflux  of  blood,  tlirough  an  incompetent  tricuspid 
valve. 

Pulsation  on  the  front  of  the  chest  may  be  produced  in  many 
ways,   for   the  heart   is   often   displaced  in  pulmonary  and 


Fia.  153. — Epigastkeo  Pxtlsation  synchronous  with  Apex  Impulse  and 
Positive:  Left  Ventricle. 

abdominal  disease,  the  viscera  may  be  transposed  or  an 
aneurism  may  be  present,  and  the  nature  of  the  pulsation  can 
only  be  recognized  by  careful  examination. 


Fia.  154. — Curves  of  Brachial  Pulse,  Pulsation  in  Second  Left  Intercostal 
Space  and  Apes  Impulse. 

The  area  of  cardiac  dulness  is  often  altered  by  pulmonary 
disease.  Under  normal  circumstances  it  is  an  inaccurate  guide 
to  the  size  of  the  heart,  for,  though  the  left  and  the  upper 


A7M,,S?t 


Fig.  155. — Pulsations  prom  Fourth  Right  Intercostal  Space  and  Apex 

Impulse. 

The  pulsation  on  the  right  side  is  inverted. 

margins  can  be  deUmited  fairly  accurately,  the  right  margin 
is  always  within  the  right  border  of  the  heart,  as  the  sternal 
note  is  representative  of  the  structures  underlying   it  as  a 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     325 


whole,  and  the  lower  margin  runs  into  the  area  of  hepatic 
dulness.  The  so-called  areas  of  superficial  and  deep  dulness 
are  notoriously  inaccurate.  A  medium  strength  of  stroke 
yields  the  best  result,  and  the  physician  must  be  careful  to  use 
the  same  technique  habitually  and  to  form  his  own  estimate  of 
the  normal  dimensions  of  the  area  (Figs.  156,  157). 

The  cardiac  dulness  in  healthy  individuals  varies  appreciably 
with  variations  in  respiration,  being  diminished  during  full 
inspiration  and  vice-versa. 
It  may  be  notably  less- 
ened in  emphysema  and 
apparently  increased  in 
pulmonary  consolidation 
and  retraction.  Absence 
of  the  physiological  varia- 
tions is  an  important  sign, 
for  it  indicates  fixation  of 
the  anterior  margins  of 
the  lungs. 

The  character  and  the 
area  of  audibility  of  the 
cardiac  sounds  and  valvu- 
lar murmurs  requires  care- 
ful examination .  The  fir s  t 
sound  is  due  to  the  con- 
traction of  the  ventricular 
muscle  and  to  the  closure 
of  the  auriculo-ventricular 
valves.  If  the  ventricle 
is  powerful,  the  sound  is 
long  and  dull,  as  the 
muscular  element  is  well-marked ;  but  if  the  muscle  is  weak,  the 
valvular  element  becomes  predominant,  and  the  sound  becomes 
shorter  and  sharper,  and  approximates  in  character  to  that  of 
the  normal  second  sound.  The  second  sounds  are  due  to  the 
closure  of  the  arterial  valves.  They  are  loud  if  the  arterial 
pressure  is  high,  and  weak  if  the  pressure  is  low,  or  the  valves 
stiff  and  immobile ;  absence  of  a  second  sound  always  indicates 
a  gross  valvular  defect.  But  the  character  of  the  sounds  may 
be  greatly  altered  by  the  thickness  of  the  overlying  structures. 


Fig. 


156. — Diagram  showing  Surface  Ee- 
LATiONs  OF  Heart  and  Lungs. 


326 


DISEASES  OE  THE  HEART 


and  they  are  often  weakened  in  fat  and  in  very  muscular 
individuals,  and  in  emphysematous  patients  ;  and  they  may  be 
loud  in  thin  people  or  in  those  Avhose  lungs  are  retracted  from 
the  front  of  the  chest,  quite  apart  from  an}^  real  alteration  in 
the  heart  itself.      The  loudness  of  valvular  murmurs  may  of 

course  be  affected  in  the 
same  way. 

The  conduction  of 
sounds  and  murmurs  is 
due    to    several   factors : 

(1)  The  site  of  production 
of  the  sound.  The  second 
sounds  are  loudest  at  the 
base  and  the  first  sounds 
over   the  ventricles. 

(2)  The  direction  of  the 
flow  of  blood  at  the  time 
when  the  murmur  is  being 
produced.  The  sj'stohc 
aortic  murmur  is  well  con- 
ducted into  the  carotid 
arter}^,  and  the  diastohc 
murmur  doi^aiwards  to- 
wards     the      ventricles . 

(3)  The  relationship  of  the 
chambers  with  which  they 
are  concerned  to  the  sur- 
face of  the  chest.  The 
left  auricle,  for  example, 

is  deeply  situated,  while  the  left  ventricle  is  relative^  superficial. 
In  mitral  stenosis  the  presystoHc  murmur  is  heard  best  at  the 
apex,  because  this  is  the  nearest  accessible  spot  to  the  mitral 
valve,  and  the  current  of  blood  which  produces  the  abnormal 
sound  is  flowing  from  auricle  to  ventricle. 

In  mitral  regurgitation,  too,  the  murmur  is  heard  best  at 
the  apex  of  the  ventricle,  though  it  must  be  louder  in  the  left 
auricle,  as  the  current  of  blood  is  flowing  from  ventricle  to 
auricle;  but  the  distance  of  the  left  auricle  from  the  front  of 
the  chest  prevents  it  being  heard  best  over  the  auricle.     The 


Fig.  157." — Diagram  showtng  Area  of  Dtjl- 
NBss  OP  Heart  astd  Liter. 

Author's  normal. 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     327 

murmur  of  stenosis  is  rarely  heard  weU  at  the  back  of  the 
€hest,  as  the  current  is  flowing  from  behind  forwards ;  and 
the  murmur  of  insufficiency  is  often  heard  weU  at  the  back, 
as  the  current  which  produces  it  is  flowing  towards  the  back 
of  the  chest. 

An  abnormal  conduction  of  sounds  or  murmurs  indicates 
some  abnormality  which  occasions  it.  In  consohdations  of  the 
middle  lobe  of  the  right  lung  the  cardiac  sounds  are  well  con- 
ducted towards  the  right  nipple.  In  aneurism  they  are  well 
conducted  to  any  region  where  the  aneurism  comes  near  the 
surface  of  the  chest.  The  conduction  of  the  cardiac  sounds 
is  thus,  like  the  area  of  cardiac  dulness,  dependent  upon  the 
condition  of  the  structures  surrounding  the  heart  almost  as 
much  as  upon  alterations  in  heart  itself. 

The  Causes  of  Murmurs. — ^The  localization  of  a  murmur 
indicates  the  site  of  the  valvular  lesion,  but  the  character  of 
the  murmur  conveys  little  information  as  to  the  grade  of  the 
defect.  Its  loudness  depends  upon  two  factors — the  nature  of 
the  lesion  and  the  rate  of  flow  of  the  current  of  blood — and  a 
murmur  may  weaken  or  even  disappear  in  cardiac  failure 
from  variations  in  the  second  factor,  without  any  change 
occurring  in  the  valve  itself.  Other  things  being  equal,  a 
loud  murmur  is  more  satisfactory  than  a  weak  murmur,  for  it 
is  indicative  of  a  powerful  cardiac  muscle. 

The  duration  of  a  murmur,  on  the  other  hand,  conveys 
definite  information  of  value .  A  mi  tral  murmur  which  obscures 
the  first  sound  and  occupies  the  whole  of  the  short  pause 
indicates  regurgitation  during  the  whole  of  ventricular  systole, 
while  a  mere  whiff  succeeding  a  distinct  first  sound  shows  that 
regurgitation  is  only  occurring  during  a  part  of  systole. 

The  character  of  a  murmur  may  alter  from  several  causes. 
In  acute  endocarditis,  and  less  frequently  in  the  chronic  disease, 
the  valve  itself  may  undergo  notable  changes.  A  cusp  may  be 
perforated  and  becom.e  notably  incompetent,  or  vegetations 
may  become  so  luxuriant  that  a  previously  existing  incom- 
petence ceases.  The  muscle  may  become  too  weak  to  produce 
audible  vibrations,  or  with  increasing  strength  may  generate 
a  longer  and  a  louder  sound.  The  cardiac  rhythm  may  change. 
This  latter  factor  has  already  been  considered  in  some  detail. 


328  DISEASES  OF  THE  HEART 

In  auricular  fibrillation  the  co-ordinate  contraction  of  the 
auricular  muscle  ceases,  and  any  murmur  produced  by  auricular 
contraction  ceases  too,  so  that  in   mitral  stenosis,  with  the 


I     ^ 

I 

m 

Aurioulap  Systole 

wm/////M///M 

W///////////////M 

Ventricular  Systole 

\  SHUT  1 

OPEN 

1  SHUT  1 

Aurioulo-Ventricular 

Valves 

1  OPEN  1 

SHUT 

1  OPEN  1 

Arterial  Valves 

1       f     n 

1       1     n 

Cardiac  Sounds 

iiiiinm  n  I liiiiiiM,.  n 

nillln,.,,  D  lllilllllllllliu.,,, D 

I 1         □ I  I        niiinin 

I  I  lllliri I  I         llliinn. 


Systolic  Murmurs 


Diastolic  Murmurs 


.-.irllilO 

D 

,1,11111(0 

D 

• 

„MlllllO 

Dliiiii 

..11111111110 

Dill, 

iiiO 

Dlllin, 

/ 

iMIIIillO 

Dliiii,, 

n 

Oiii. 

Q 

Diiiiii 

Presystolic  Murmur 

Full  Diastolic  Murmur 

Early  Diastolic  and 
Presystolic  Murmurs 

Early  Diastolic  Murmur 

Pig.  158. — Diagram  showing  the  Time  Relations  of  the  Cabdiac  Contrao. 
TioNS,  THE  Cardiac  Sotxnds  and  Valvular  Murmurs,  and  the  Corre- 
sponding Condition  of  the  Cardiac  Valves. 

onset  of  fibrillation,  the  presystolic  murmur  disappears.  Re- 
gurgitation in  mitral  incompetence  can  be  only  minimal  if  the 
auricle    and   ventricle   contract    simultaneously,    so    that    in 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     329 

heart-block,  partial  or  complete,  and  in  extra-systoles,  the 
duration  and  loudness  of  a  murmur  may  vary  with  successive 
beats ;  while  in  nodal  rhythm  and  in  paroxysmal  tachycardia 
a  systohc  mitral  murmur  may  be  constantly  weakened  or  may 
disappear  altogether. 

The  presence  of  a  murmur  does  not  necessarily  indicate 
structural  disease  of  the  valve.  The  arterial  valves  are  simple 
mechanical  contrivances  which  probably  act  independently  of 
muscular  action  (cf.  p.  299),  but  the  auriculo-ventricular  valves 
are  in  large  measure  closed  by  contraction  of  their  muscular 
sphincter,  and  may  become  incompetent  from  muscular  weak- 
ness without  any  abnormality  of  the  cusps.  Mitral  and  tri- 
cuspid reflux  may  thus  be  temporarj^  if  the  muscular  weakness 
is  due  to  removable  causes.  "Curable  "  mitral  reflux  can  be 
recognized  by  the  absence  of  any  of  the^f actors  which  produce 
valvular  disease,  and  by  the  presence  of  conditions  which 
produce  weakness  of,  or  throw  strain  upon,  the  ventricular 
muscle.  Debilit}^,  anaemia,  etc.,  represent  the  former;  physical 
strain  and  aortic  valvular  disease  the  latter. 

Murmurs  are  not  infrequently  present  in  patients  whose 
cardiac  valves  are  normal.  They  are  always  systohc  in  rhythm, 
but  may  be  of  various  characters — soft  or  harsh,  loud  or  weak, 
long  or  short ;  and  thej  may  be  present  over  any  part  of  the 
cardiac  area.  According  to  the  late  Dr.  Sansom,  the  most 
frequent  site  is  over  the  pulmonary  artery-  and  the  conus 
arteriosus  in  the  second  and  third  left  interspaces  close  to  the 
sternum  (59  per  cent.).  They  may  be  heard  in  the  aortic  area 
(11  per  cent.),  and  at  the  apex  (7  per  cent.) ;  and  may  be  present 
over  the  conus  arteriosus  and  right  ventricle  (11  per  cent.); 
and  at  both  the  apex  and  the  pulmonary  area  (9  per  cent.). 
The  most  frequent  causes  are  anaemia  and  post-febrile  debility ; 
and  they  may  also  occur  in  excited  hearts  (as  in  Graves's 
disease),  in  women  following  child-birth,  and  in  any  case 
where  the  heart  is  displaced  from  its  usual  site  by  pleural 
effusions,  abdominal  distension,  etc. ;  they  are  generallj'  present 
in  extreme  lateral  curvature  of  the  spine.  The  apical  murmur 
is  probably  always  a  sign  of  mitral  reflux.  The  basal  murmurs 
are  probably  produced  in  the  aorta  or  the  pulmonary  artery,  as 
the  case  may  be,  and  may  well  result  from  kinking  of  the  vessel 


f^30  DISEASES  OF  THE  HEART 

in  cases  where  the  heart  is  displaced;  but  their  origin  in  other 
cases  is  unknown,  though  numerous  theories  have  been  suggested. 
Their  recognition  is  usually  easy.  Organic  disease  of  the 
pulmonary  valve  is  very  rare  save  in  congenital  heart  disease, 
in  which  the  disturbance  of  the  circulation  is  usually  con- 
siderable, and  clubbing  of  the  finger-tips,  cyanosis,  or  other 
congenital  defects,  often  co-exist;  the  right  heart,  too,  is 
generally  enlarged  in  consequence  of  the  excessive  strain 
thrown  upon  it.  Aortic  stenosis  without  regurgitation  is 
unusual,  though  a  systolic  murmur  is  not  uncommon  in  later 
life,  as  the  result  of  some  stiffening  or  roughness  of  the  cusps 
unaccompanied  by  definite  narrowing  of  the  orifice ;  in  this  case 
the  second  sound  is  generally  abnormal,  and  emphatic  or 
intoned  or  weakened,  and  the  left  ventricle  is  more  or  less 
hypertrophied.  So  that  in  the  presence  of  a  systolic  basal 
murmur  as  an  isolated  sign  the  presumption  is  against  the 
presence  of  organic  disease.  Obvious  causes  of  functional 
murmurs,  too,  are  usually  apparent,  and  the  bruit  de  diable  is 
frequently  heard  on  auscultation  over  the  jugular  vein.  The 
size  of  the  heart  is  rarely  increased,  and  the  second  sounds  are 
of  normal  character.  The  murmur  is  usually  not  loud,  and  is 
badly  conducted,  and  is  variable  or  perhaps  inconstant,  accord- 
ing to  the  attitude  of  the  patient  and  the  phase  of  respiration. 
It  is  almost  always  best  marked  when  the  patient  is  recumbent, 
and  less  distinct  or  absent  when  he  assumes  the  upright 
position ;  and  it  can  often  be  altered  by  the  cessation  of  respira- 
tion, either  on  full  inspiration  or  full  expiration ;  while  it  may 
only  be  present  when  the  patient  is  at  rest,  disappearing  on 
even  shght  exertion.  A  similar  variability  ma}^  also  occur 
with  the  apical  systolic  murmur.  As  a  rule  this  murmur 
observes  all  the  distinctions  which  connote  the  presence  of 
mitral  regurgitation,  though  it  disappears  when  the  patient's 
health  and  the  tone  of  the  muscular  sphincter  are  restored. 
In  other  instances,  however,  the  murmur  itself  is  suggestive 
of  a  functional  cause,  being  most  distinct  outwith  or  inside 
the  apex  impulse  and  not  over  it,  and  varying  with  the  respira- 
tory phases,  waxing  during  inspiration  and  waning  during  ex- 
piration. Cessation  of  respiration  on  full  expiration  generally 
causes  this  murmur  to  disappear  (carclio-pulmonary  murmur). 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     331 

Too  much  reliance,  however,  must  not  be  laid  upon  the 
-auscultatory  signs,  and  the  case  must  be  considered  on  general 
lines.  The  presence  at  the  time,  or  previously,  of  any  disease, 
:such  as  acute  rheumatism,  which  is  commonly  accompanied 
by  endocarditis,  always  turns  the  bias  in  favour  of  organic 
•disease  of  the  valve. 

The  Physical  Signs  oJ  Myocardial  Weakness  in  the  Infections. 

— The  physical  signs  of  chronic  myocardial  failure  are  some- 
times slight  and  equivocal,  for  they  are  often  disturbed  by 
pre-existing  changes  in  the  heart.  The  apex  impulse  in  renal 
cirrhosis,  for  example,  may  be  more  forcible  than  normal, 
though  it  is  really  weak  for  the  individual  case.  The  borders 
of  the  area  of  cardiac  dulness  may  be  displaced  on  account  of 
compensator}^  enlargement,  and  not  from  the  dilatation  of 
progressive  weakness.  And  the  cardiac  sounds  may  be  weak 
or  distant  from  emphysema  or  subcutaneous  fat.  The  pulse, 
too,  may  convey  erroneous  ideas,  for  its  rate  is  not  necessarily 
increased  in  failure,  and  it  may  be  less  frequent  than  the 
•average,  and  the  blood-pressure  may  be  above  the  normal, 
though  too  low  for  the  individual's  comfort.  The  history  of 
the  case  and  the  nature  of  the  symptoms  are  the  most  useful 
/guide  in  both  diagnosis  and  prognosis. 

The  physical  signs  of  increasing  cardiac  weakness  are  well 
seen  in  the  injections,  in  particular  those  without  local  cardiac 
lesions  and  of  severe  character,  such  as  typhus  fever,  for 
appreciable  changes  may  occur  in  the  course  of  a  few  hours, 
and  so  at  a  time  when  the  memory  of  their  former  character 
is  acute  and  accurate. 

The  apex  impulse,  as  the  weakness  increases,  loses  its  punc- 
tate character  and  becomes  more  diffuse,  while  its  force  and 
•duration  diminish,  until  it  wholly  disappears .  It  can,  however, 
often  be  recovered  if  the  patient  lies  on  his  left  side,  but  may 
«ven  then  be  lost  if  the  weakness  is  extreme.  The  area  of 
dulness  is  rarely  appreciably  altered,  but  shght  variations  in 
the  position  of  the  various  borders  may  sometimes  be  deter- 
mined. The  auscultatory  signs  are  more  distinct.  The  first 
apical  sound  loses  its  special  emphasis  and  becomes  less 
loud  and  more  distant,  its  quality  is  altered,  and  it  becomes, 


332  DISEASES  OF  THE  HEART 

shorter  and  sharper  and.  approximates  to  that  of  the  second 
sound;  so  that,  if  the  heart  is  beating  freqluently  and  diastole 
is  shortened,  the  sounds  closely  resemble  the  tic-tac  of  the 
watch  or  the  foetal  heart.  The  change  is  best  appreciated 
at  the  apex,  where  the  first  sound  is  normally  loudest  and  most 
emphatic ;  with  its  weakening  the  second  sound  becomes 
relatively  loud,  and  so  apparently  accentuated.  The  sounds 
at  the  base  are  similarly  affected,  but  as  the  second  sound  here 
is  in  health  the  loudest,  the  alteration  is  less  readily  recog- 
nized. The  first  sound  may  finally  disappear  at  the  base^ 
though  it  is  still  audible  at  the  apex;  and  eventually  may  be 
inaudible  anywhere.  The  pulse-rate  as  a  rule  becomes  more 
frequent  with  increasing  weakness,  and  though  the  amphtude 
of  the  wave  is  not  at  first  affected,  its  force  and  duration  are 
lessened,  and  it  becomes  softer  and  quicker,  and  perhaps 
dicrotic ;  eventually  it  becomes  smaller  as  well.  The  rhythm 
of  the  pulse  is  occasionally  changed.  An  inJrequent  pulse  in  a 
febrile  illness  is  generally  due  to  a  coupled  rhythm,  the  extra- 
systolic  beat  being  imperceptible  to  the  finger,  though  it  can 
be  recognized  on  auscultation.  The  irregularities  due  to  extra- 
systoles,  heart-block,  auricular  fibrillation,  and  auricular 
flutter,  may  all  occur,  though  they  are  uncommon  even  in  cases 
where  an  acute  endocarditis  has  ensued,  but  I  have  observed 
them  all  in  pneumonia  and  acute  rheumatism.  Greoffrey 
Fleming  has  been  kind  enough  to  give  me  some  statistics 
(unpublished)  upon  this  point,  the  result  of  his  investigations 
in  RuchiU  Fever  Hospital.  Of  29  cases  (diphtheria,  10; 
scarlatina,  9 ;  enteric  fever,  7 ;  typhus  fever,  3),  where  routine 
tracings  were  taken  from  the  second  or  third  day  of  the  illness,. 
2  alone  showed  extra-systoles,  and  they  occurred  in  only  5  out 
of  61  patients  suffering  from  various  fevers,  in  whom  tracings 
were  taken  on  account  of  some  cardiac  abnormahty.  Heart- 
block  was  detected  in  1  case  of  diphtheria,  in  which  the  a.v, 
bundle  was  afterwards  found  to  be  involved  in  an  inflammatory 
lesion;  and  in  another  case  of  diphtheria,  a  case  of  enteric 
fever,  and  a  case  of  scarlatina,  a  transient  partial]  block  was 
recognized. 

The  Physical  Signs  o£  Mitral  Disaase. — The  general  appear- 
ance of  mitral  patients  is  often  suggestive,  but  is,  of  course, 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     333 

■only  apparent  in  patients  with  advanced  disease.  The  face  is 
puffy  and  congested,  and  the  complexion  is  dusky,  and  the 
lips  and  ears  are  more  or  less  blue.  A  malar  flush  is  common, 
and  the  malar  capillaries  may  be  permanently  dilated.  The 
hands  and  feet  are  often  cold  and  clammy,  and  in  chronic 
cases  a  mild  degree  of  clubbing  of  the  finger-tips  may  be  found. 
Difficulty  in  respiration,  too,  may  be  evident  even  when  the 
patient  is  at  rest. 

Mitral  Stenosis. — The  apex  impulse  is  punctate  and  not 
well  defined,  and  little,  if  at  all,  displaced ;  it  may  be  impalpable. 
Pulsation  is  often  present  in  the  second  left  intercostal  space 
■close  to  the  sternum,  and  in  the  epigastrium.  There  has  been 
much  discussion  as  to  the  cause  of  the  former  pulsation.  George 
BaKour  maintained  that  it  was  due  to  the  dilated  left  auricle  en- 
larging forwards  in  front  of  the  pulmonary  artery  and  reaching 
the  front  of  the  chest.  This  undoubtedly  does  occur,  but  it  is 
rare  (I  have  only  seen  one  example  post-mortem),  while  the 
pulsation  in  question  is  of  common  occurrence.  It  is  generally 
due,  as  William  Russell  has  shown,  to  enlargement  of  the 
pulmonary  artery  or  of  the  conus  arteriosus,  the  left  auricle 
seldom  presenting  more  than  the  tip  of  the  appendix  on  the 
front  of  the  heart,  and  it  is  outside  the  pulmonary  artery 
and  well  away  from  the  sternum.  In  polygraph  tracings 
[cf.  Fig.  154)  the  chief  wave  usuaUy  succeeds  the  apex  impulse, 
and  is  undoubtedly  derived  from  the  pulmonary  artery,  though 
a  smaller  wave  of  auricular  rhythm  often  co-exists.  Occasion- 
ally the  chief  wave  is  synchronous  with  the  apex  impulse,  and 
presumably  due  to  the  contraction  of  the  conus.  The  epigas- 
tric pulsation  is  generally  inverted,  and  therefore  due  to  the 
contraction  of  the  right  ventricle. 

In  certain  cases  of  mitral  stenosis  the  apex  impulse  is  large 
and  well  marked,  and  may  be  considerably  displaced  both 
outwards  and  downwards.  This  may  result  from  the  co- 
existence of  mitral  reflux  or  disease  of  the  aortic  valve,  which 
necessarily  entail  enlargement  of  the  left  ventricle.  When  it 
obtains  without  mitral  reflux  or  aortic  disease,  it  is  invariably 
associated  with  a  high  blood-pressure  and  arterio  sclerosis  or 
fibroid  kidneys.  In  some  of  these  cases  the  epigastric  pulsa- 
tion is  due  to  the  left  ventricle;  careful  examination  of  the 


334 


DISEASES  OF  THE  HEART 


rhythm  of  the  pulsation  -will  decide  the  point.     The  sternum^ 
too,  may  definitely  pulsate. 

The  thrill  is  very  characteristic,  and  is  frequently  present. 
It  commences  during  diastole  as  a  soft,  purring  tremor,  and 


Fig. 


159. — Skiagram:  Reis^al  Cirrhosis,  Hypertrophy  of  Left  Ventricle 
(c/.  Fig.  162)  (J.  R.  R.). 


rapidly  increasing  in  intensity,  ends  abruptly  as  the  apex 
impulse  reaches  the  hand.  It  is  usually  limited  to  the  imme- 
diate vicinity  of  the  apex,  but  it  is  sometimes  widespread,  and 
I  have  felt  it  distinctly  beneath  the  xiphoid  cartilage,  though 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     335 


post-mortem  the  tricuspid  valve  was  not  narrowed.  In  another 
case  in  which  the  same  distribution  was  present,  tracings  showed 
that  the  epigastric  pulsation  was  due  to  the  left  ventricle,  the 
chest  being  long  and  narrow,  and  the  left  ventricle  hyper- 
trophied  and  powerful. 

The  area  of  dulness  is  as  a  rule  but  little  altered.  In  some 
cases  it  is  enlarged  to  the  right  from  dilatation  of  the  right 
heart,  or  upwards  along 
the  left  side  of  the  ster- 
num, even  as  high  as  the 
second  costal  cartilage, 
from  dilatation  of  the 
conus  or  the  pulmonary 
artery  (Fig.  160). 

The  murmur  is  diastolic 
(presystolic)  in  rhythm, 
and  at  first  soft  and 
distant  ;  but  it  rapidty 
becomes  loud  and  rough 
(crescendo),  terminating 
abruptly  with  a  loud 
"snap,"  the  shortened 
representative  of  the  first 
sound.  It  is  well  imitated 
b}^  vocalizing  the  symbols 
rrrh  or  voot.  The  exact 
cause  of  the  murmur  has 
been  much  disputed.  It 
commences  during  ven- 
tricular diastole  and  ends 
synchronously  with  the 
apex  impulse,  and  thus 
occurs  during  the  period  of  auricular  systole.  It  is  one  of  the 
loudest  and  roughest  of  cardiac  murmurs,  and  it  seems  im- 
possible that  it  can  be  produced  by  the  relatively  weak  auricular 
systole;  but  its  chief  cause  is  undoubtedly  auricular,  for  it 
disappears  when  auricular  fibrillation  occurs.  Other  factors, 
however,  aid  in  its  production. 

In  its  typical  form  the    murmur  begins  early  in  diastole, 


Fig.  160. — Diagraivi  showing  Area  of  Dtjl- 
btess  and  pulsation  ( +  )  in  mlteal 
Stenosis. 

This  and  the  following  diagrams  are  actual 
ease  records  from  my  ward  journals. 


336  DISEASES  OF  THE  HEART 

and  so  softly  tliat  the  exact  commencement  is  difficult  to  deter- 
mine; the  "snap  "  with  which  it  ends  is  synchronous  with  the 
apex  impulse.  The  apex  impulse,  however,  is  not  exactly 
synchronous  with  the  commencement  of  ventricular  systole, 
for  a  certain  period  elapses  before  the  muscular  contraction 
so  alters  the  shape  and  position  of  the  ventricles  that  the 
impulse  is  perceptible  outside  the  chest  wall.  The  early  parts 
of  the  murmur,  therefore,  are  diastohc  in  time,  while  the  ter- 
minal crescendo  portion  is  synchronous,  first  of  all  with 
auricular  systole,  and,  at  the  very  end,  with  the  commence- 
ment of  ventricular  systole.* 

The  mechanical  disturbance  in  mitral  stenosis  is  peculiar 
to  this  lesion.  The  obstruction  at  the  valve  leads  to  engorge- 
ment within  the  left  auricle,  and  its  muscle  in  consequence 
hypertrophies,  but  as  this  is  rarely  sufficient,  the  left  auricle 
dilates,  the  pulmonary  circulation  becomes  engorged,  and  the 
right  ventricle  in  consequence  hypertrophies.  At  the  con- 
clusion of  ventricular  systole  the  left  ventricle  is  relatively 
empty  and  the  intraventricular  pressure  is  at  a  minimum,  while 
the  auricular  (left)  pressure  is  relatively  high,  as  the  chamber 
has  just  been  refilled  from  the  right  heart.  If,  from  the  rela- 
tive difference  in  pressure  within  the  two  cavities,  the  fiow  of 
blood  is  rapid,  a  soft  murmur  may  be  produced.  In  mid- 
diastole  the  difference  in  pressure  is  less,  for  the  ventricle  is  now 
partly  filled  and  the  auricle  partly  emptied,  and  the  flow  is  less 
rapid  and  the  murmur  becomes  more  faint  or  disappears. 
When  auricular  systole  ensues,  the  difference  in  pressure  is 
rapidly  augmented,  the  flow  becomes  more  rapid,  and  the 
murmur  becomes  louder.  At  the  commencement  of  ventricular 
systole  the  intraventricular  pressure,  on  account  of  the  mitral 
obstruction,  is  stiU  relatively  low,  and  the  auricular  pressure  is 

*  The  time  relations  of  the  commencement  of  ventricular  systole  and  the 
first  sound  of  the  heart  have  been  investigated  by  means  of  the  phono-electro- 
cardiograph, and  it  is  stated  by  Fahr,i  that  the  former  precedes  the  latter  by 
0-02  to  0-04  second.  Weiss  and  Joachim,^  using  similar  methods,  have  found 
that  the  terminal  portion  of  the  crescendo  murmur  occurs  during  ventricular 
systole.     Lewis's  conclusions^  are  similar. 

1  Heart,  1912,  vol.  iv.,  p.  147. 

2  Zeitschr.f.  Bin.  lied.,  1910,  vol.  siii. 

3  Heart,  1913,  vol.  iv.,  p.  241. 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     337 


still  relatively  high,  and  until  the  ventricular  pressure  rises 
above  the  auricular  pressure  as  the  result  of  ventricular  con- 
traction, the  valve  will  not  be  closed,  and  blood  will  continue 
to  flow  from  auricle  into  ventricle.  This,  of  course,  only 
occurs  for  a  very  short  period,  as  the  intraventricular  pressure 
rises  very  rapidly,  but,  synchronously  with  the  commencement 
of  ventricular  systole, 
the  sphincter  muscle  of 
the  mitral  valve  and  the 
muscuH  papillares  con- 
tract, so  that  the  shape 
of  the  valve  and  the  ten- 
sion of  its  cusps  are 
altering  while  blood  is 
still  flowing  from  auricle 
into  ventricle;  and  it  is  just 
at  this  moment  that  the 
characteristic  crescendo 
part  of  the  murmur  oc- 
curs. As  the  current 
ceases  to  flow,  the  "snap  " 
is  heard.  The  crescendo 
character  then  is  due  to 
blood  flowing  through  the 
mitral  valve  at  a  time 
when  changes  are  taking 
place  in  the  lumen  of  the 
orifice  and  in  the  tension 
of  the  cusps,* 

The  influence  of  the 
ventricular  contractions 
is  shown  as  weU  by  another  phenomenon.  In  slight  degrees 
of  mitral  stenosis  the  murmur  may  be  absent  when  the  patient 
is  lying  down,  but  becomes  distinct  on  any  physical  exertion. 
such  as  sitting  up,  an  action  which  has  a  definite  effect  on  the 
strength  of  the  ventricular  contraction,  and  but  little  effect 
upon  the  contraction  of  the  auricle. 

The  crescendo  murmur  is  usually  heard  best  a  little  internal 
*  Cowan,  Glasgow  Med.  Journ.,  1898,  vol.  xlix.,  p.  166. 


Fig.  161. — Diagbat^i  showing  Distribution 
OF  Pkesystolic  Mtjrmtjk  (0)  IN  Mitral 
Stenosis. 

fl  =  accentuation  of  second  pulmonic 
sound. 


338 


DISEASES  OF  THE  HEART 


to  and  above  the  apex  impulse,  and  is  limited  in  its  distribu- 
tion, being  generally  audible  over  an  area  which  is  little  larger 
than  a  crown  piece  (Fig.  161).  The  limited  area  of  audibility 
is  proportionate  to  the  area  of  left  ventricle  related  to  the 


Fig. 


162. — Skiagram:   Mitral  Stenosis.  Dilatation  and  Hypertrophy  of 
Right  Heart  (J.  R.  R.)  (c/.  Fig.  159). 


front  of  the  chest,  which,  in  uncomphcated  cases,  is  small,  as 
the  enlarged  right  ventricle  displaces  the  left  backwards  and 
away  from  the  front  of  the  chest ;  but  the  area  is  larger  when 
the  left  ventricle  is  enlarged  from  other  causes,  and  the  murmur 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     339 

may  then  be  audible  right  up  to  the  sternum.  The  murmur  is 
rapidly  lost  towards  the  axilla,  though  the  softer  systolic 
murmur  is  weU  conducted  in  this  direction.  The  reason 
is  obvious.  In  mitral  reflux  the  ventricle  is  in  systole,  and 
the  apex  is  in  intimate  contact  with  the  ribs,  and  the  vibra- 
tions are  well  conducted  along  them.  In  mitral  stenosis  the 
murmur  is  diastolic  in  rhythm,  the  apex  is  not  firmly  applied 
to  the  chest,  and  the  vibrations  are,  in  consequence,  rapidly 
lost. 

If  auricular  fibrillation  ensues,  the  early  diastohc  murmur 
may  persist,  though  the  characteristic  presystohc  murmur 
disappears ;  for  when  the  co-ordinated  auricular  contraction 
ceases,  the  flow  of  blood  at  the  end  of  diastole  is  not  sufficiently 
rapid  to  produce  audible  vibrations.* 

If  the  ventricle  is  relatively  weak,  the  early  diastohc  murmur 
rapidly  succeeds  the  second  sound  and  quickly  dies  away 
(lubb-te-te),  simulating  a  doubled  second  sound,  but  differing 
from  true  doubhng  in  its  distribution,  the  latter  being  heard 
best  at  the  base,  the  former  only  at  the  apex  (Figs.  163,  164). 
If  the  ventricle  is  powerful,  the  diastolic  aspiration  may  be 
powerful,  and  the  murmur  may  be  of  considerable  duration. 
The  murmur  is  necessarily  separated  from  the  second  sound, 
for,  as  Lewis  pointed  out,  the  auriculo-ventricular  valve  only 
opens  after  the  aortic  valve  has  closed. 

The  third  murmur  of  mitral  stenosis  is  of  different  origin. 
It  is  a  soft  murmur  of  varying  length,  running  out  of  the 
second  sound,  and  heard  best  to  the  left  of  the  sternum  in  the 
second  or  third  interspace.  It  is  almost  certainly  due  to 
relative  incompetence  of  the  pulmonary  valves,  the  pulmonary 

*  James  Mackenzie  has  pointed  out  that  the  presystolic  murmur  may  also 
disappear  if  conductivity  is  defective  and  the  auricular  and  ventricular  con- 
tractions are  separated  from  their  usual  close  connect!  on.  Ritchie!  has  demon- 
strated this  in  electro- cardiograms  (Fig.  67).  I  have  observed  it  in  one  case 
where  the  murmur  was  absent  when  the  a-c  interval  measured  0-25  second,  and 
present  when  the  interval  measured  0-20  second.  A  mid- diastolic  murmur 
synchronous  with  auricular  systole,  and  separate  from  both  first  and  second 
sounds,  may  appear  in  these  cases,  and  has  been  demonstrated  by  Lewis^  with 
the  phono-electro-cardiograph. 

1  Edin.  Med.  Journ.,  1913,  vol.  x.,  N.S.,  p.  410. 

2  Heart,  1913,  vol.  iv.,  p.  241. 


340 


DISEASES  OF  THE  HEART 


artery  having  dilated  under  the  stress  of  the  increased  pressure 
within  it  to  such  a  degree  that  the  cusps  are  unable  to  close  the 
aperture. 

The  second  pulmonic  sound  in  well-compensated  cases  is 
alwaj^s  notably  emphatic,  and  may  be  palpable.  As  compen- 
sation fails  with  dilatation  of  the  right  heart,  it  loses  emphasis. 
Very  often  the  two  second  sounds  are  not  synchronous,  and 


Fig.  163.— Diagram  showing  Area 
OF  Reduplicated  Second  Sound. 


Fig.  lei. — Diagram  showing  Area  of 
Early  Diastolic  Mitral  Murjiur. 


a  '*  reduplication  "  is  audible  over  the  sternum,  which  may  be 
heard  in  lessened  intensity  at  the  apex. 

The  'pulse  in  mitral  stenosis  is  in  no  waj-  characteristic.  In 
simple  uncomplicated  cases  it  is  quite  normal  so  long  as  com- 
pensation is  good ;  but  in  manj^  cases  it  is  small  and  hard  and 
well  sustained  from  associated  renal  disease — a  complication 
which  is  present  in  a  large  proportion  of  cases,  particularly 
those  of  some  duration  (Figs.   165,    166;  c/.  p.   269).     When 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     341 


auricular  fibrillation  ensues,  the  characteristic  irregular  pulse 
makes  its  appearance,  and  generally  persists  until  the  end.  The 
blood-pressure  as  a  rule  falls  to  some  extent  when  this  occurs. 
.■'  In  mitral  stenosis  com- 
pensation is  at  first  effected 
by  hypertroph.}^  of  the  left 
auricle.  In  the  lesser  grades 
this  may  be  sufficient,  but 
in  even  average  cases  it  soon 
fails,  and  the  cavity  in  con- 
sequence dilates,  with  re- 
sultant stasis  and  congestion 
of  the  pulmonary  circuit;  to 
overcome  this  the  right 
ventricle  hypertrophies.  It 
is  difficult  to  appreciate  the 
precise  degree  of  the  lesion, 
for  the  size  of  the  left  auricle 
and  of  the  right  ventricle  can 
rarely  be  measured.  Any 
notable  increase  in  the  area 
of  dulness  to  the  right  indi- 
cates an  enlarged  right  heart 
(Fig.  167),  and  the  stenosis 
in  these  cases  is  usually  con- 
siderable; but  an  enlarged 
right  heart  is  only  present 
when  the  right  ventricle  has 
dilated  under  the  strain,  and 
compensation  is,  in  conse- 
quence, more  or  less  broken. 
Notable  epigastric  pulsation 
and  an  indistinct  apex  im- 
pulse result  from  right  ven- 
tricular hypertrophy ;  but 
other  causes 


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as  the}'  may  also  occur  from 
an  accurate  conclusion  is  difficult  to  obtain. 
If  the  right  ventricle  is  powerful,  the  lower  end  of  the  sternum 
may  be  felt  to  pulsate ;  but  this  depends  in  great  measure  on 
the  softness  of  the  ribs,  and  is  seldom  w^ell  marked  save  in 


342 


DISEASES  OF  THE  HEART 


childhood  and  in  adolescence.  It  must  be  remembered  that 
mitral  stenosis  'per  se  exerts  no  influence  upon  the  left  heart, 
which,  if  hypertrophied,  is  hypertrophied  from  other  causes. 

Mitral  Reflux. — The  apex  impulse  is  diffuse  and  heaving, 
and  is  displaced  to  the  left  and  downwards ;  it  may  be  felt  in 
several  interspaces,  and  pulsation  is  usually  also  evident  in 
the  epigastrium.  A  thrill  is  sometimes  felt  at  the  apex ;  it  is 
diminuendo  in  character,  and  accompanies  and  succeeds  the 
apex  impulse;  it  is  more  often  absent  than  present.     The  area 


DEC 


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180 
170 
160 
150 
140 
130 
120 
no 
100 
90 
80 
70 


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Fig.  166. — Blood-Peessuee  Chart. 
F.,  aged  46:  Mitral  disease;  cirrhotic  kidneys. 

of  dulness  is  increased  to  the  left  and  downwards  in  correspond- 
ing proportion  to  the  displacement  of  the  apex  (Fig.  168).  The 
murmur  is  systoHc  in  rhythm,  and  replaces  or  follows  the  first 
sound.  It  is  usually  soft  and  blowing,  and  is  less  harsh  than 
the  aortic  systoHc  murmur.  It  is  heard  best  at  the  apex,  and 
is  well  conducted  into  the  axilla  along  those  ribs  with  which 
the  apex  is  in  contact  (Fig.  169).  When  the  murmur  is  loud, 
it  may  be  audible  all  over  the  left  chest ;  and  it  is  often  distinct 
at  the  back,  with  maximal  intensity  at  the  angle  of  the  left 
scapula,  and  in  a  lessened  degree  along  the  spine  (Fig.  170).  The 
second  pulmonic  sound  is  emphatic.     The  second  sound  at  the 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     343 

base  may  be  doubled,  but  this  is  more  frequent  in  stenosis 
than  in  regurgitation. 

The  j)ulse  is  normal  in  character  in  simple,  well-compensated 
cases,  but  is  well  sustained  if,  as  frequently  happens,  renal 
fibrosis  co-exists.  When  auricular  fibrillation  ensues,  the 
characteristic  irregular  pulse  makes  its  appearance.  The 
blood-pressure  in  simple,  well-compensated  cases  is  about,  or 


Fig.  167.— Diagram  showing  Area  of 
DuLNESs  IN  A  Dilated  Heart. 


Pig.  168. — Diagram  showing  Area  op 
dulness  and  pulsation  in  mitral 
Reeltjx. 


sHghtly  below,  the  normal  reading.  In  cases  where  renal 
fibrosis  or  arterio-sclerosis  co-exist,  the  pressure  is  elevated, 
sometimes  to  very  high  readings ;  it  is  generally,  but  not  in- 
variably, high  in  the  presence  of  oedema. 

The  murmur  sometimes  shows  notable  variations  in  its 
character  with  successive  beats.  This  is  particularly  the  case 
in  heart-block  {q.v.)  when  the  auricular  and  the  ventricular 
contractions    coincide,    as    regurgitation   is    prevented    or    is 


344 


DISEASES  or  THE  HEART 


minimal;  and  the  murmur  is,  in  consequence,  absent,  or 
weakened  and  shortened.  A  similar  phenomenon  may  occur 
in  auricular  fibrillation,  for  as  the  degree  of  distension  of  the 
auricle  when  its  co-ordinated  contractions  cease  depends 
upon  the  duration  of  diastole  and  the  aspiratory  action  of  the 
left  ventricle,  it  may,  if  the  ventricular  contractions  are  fre- 


FlG.    169. — DiAGBAM  SHOWING  DISTRIBU- 
TION OP  Systolic  Murmur  in  Mitral 

E.EFLUX. 

fi= accentuation  of  second  pulmonic  sound. 


Fig.  170. — Diagram  showing  Distribu- 
tion OF  Systolic  Murmur  of  Mitral 
Reflux. 


quent,  become  so  distended  that  free  regurgitation  is  impos- 
sible. A  similar  explanation,  too,  accounts  for  the  frequent 
absence  of  a  regurgitant  murmur  in  well-marked  cases  of  mitral 
stenosis,  where  post-mortem  the  valve  is  seen  to  be  so  hard 
and  shrunken  that  the  orifice  can  hardly  be  closed,  even  if 
considerable  force  is  exerted.  The  obstruction  in  these  cases 
is  often  extreme,  and  the  congestion  in  the  auricle  too  great 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     345 

to  allow  any  appreciable  reflux  from  the  ventricle  during 
ventricular  systole. 

Mitral  regurgitation  is  compensated  by  alterations  in  the  left 
auricle  and  ventricle,  and  in  the  right  ventricle.  The  capacity 
of  the  left  ventricle  is  necessarily  increased,  for,  if  blood  flows 
back  through  the  mitral  valve  during  ventricular  systole,  the 
ventricle  must  enlarge  to  accommodate  the  amount  returned 
into  the  auricle  as  well  as  the  normal  amount  for  the  aorta ;  and 
the  Avail  is  hypertrophied  on  account  of  the  extra  work  which 
is  entailed.  During  ventricular  systole  the  left  auricle  is  over- 
distended,  for  it  receives  blood  from  the  left  ventricle  as  weU  as 
from  the  right,  and  the  auricular  wall,  in  consequence,  hypertro- 
phies. The  right  ventricle,  too,  hypertrophies,  as  its  work  is  in- 
creased by  the  heightened  pressure  within  the  pulmonary  circuit , 

The  degree  of  the  lesion  maj-  be  gauged  by  the  degree  of 
enlargement  of  the  left  ventricle.  The  length  of  the  murmur, 
too,  is  of  value  in  this  respect,  as  a  short  murmur  occurring 
after  the  first  sound  indicates  a  short  duration  of  the  regurgita- 
tion, and,  in  consequence,  a  minimal  leak.  If  the  murmur  is 
well  heard  at  the  scapular  angle,  the  lesion  is  probably  always 
organic  and  gross,  for  it  is  only  conducted  in  this  direction  in 
cases  where  the  left  auricle  is  dilated  and  reaches  close  to  the 
back;  and  this  will  not  occur  in  slight  or  in  functional  in- 
sufficiency. In  well-marked  regurgitation  the  second  pulmonic 
sound  is  notably  emphatic.  If  the  right  ventricle  is  greatly 
hypertrophied,  the  lower  end  of  the  sternum  may  pulsate,  and 
epigastric  pulsation  is  well-marked.  The  relationship  between 
the  size  and  strength  of  the  pulse  and  the  apex  impulse  should 
also  be  compared,  for  in  well  marked  regurgitation  the  pulse 
is  small  and  soft,  though  the  apex  impulse  is  diffuse  and  powerful. 

In  cases  of  mitral  disease  where  compensation  has  failed,  the 
physical  signs  may  alter.  The  pulsation  in  the  apex  region 
becomes  more  diffuse  and  less  powerful,  and  is  often  better 
seen  than  felt,  and  is  not  well  sustained.  Epigastric  pulsation  is 
more  marked,  and  pulsation  may  be  felt  in  the  fourth  and  fifth 
right  intercostal  spaces.  The  area  of  dulness  is  increased  both 
to  the  left  and  to  the  right.  The  murmurs  become  shorter  and 
less  loud,  and  the  second  pulmonic  soundless  emphatic  ;  reduphca- 


346  DISEASES  OF  THE  HEART 

lion  generally  persists.  If  auricular  fibrillation  has  ensued,  the 
crescendo  thrill  and  murmur  of  stenosis  disappear,  though  the 
early  diastohc  murmur  may  persist.  The  pulse  becomes  more 
frequent  and  the  wave  loses  in  strength,  volume,  and  duration. 

The  Physical  Signs  of  Aortic  Disease. — The  general  appear- 
ance of  aortic  patients  may  be  characteristic.  They  are  often 
notably  pale,  and  may  appear  careworn  or  anxious,  frightened 
or  in  pain;  the  carotid  or  the  temporal  arteries  may  visibly 
pulsate,  and  the  head  may  shake  with  each  beat  of  the  heart. 
These  symptoms,  however,  must  be  referred  more  frequenth^ 
to  associated  disease  than  to  the  valvular  lesion  itself;  for 
while  anaemia  occurs  in  aortic  valvular  disease,  it  only  obtains 
when  the  compensatory  arrangements  have  broken  down  and 
the  general  nutrition  is,  in  consequence,  defective.  Anaemia 
occurs  in  syphihs,  in  arterio-sclerosis,  and  in  chronic  renal 
disease,  and  its  presence  in  aortic  valvular  disease  is  most  often 
due  to  those  causes,  and  not  to  the  cardiac  lesion.  Anaemia  is 
by  no  means  constant;  some  aortic  patients  are  plethoric 
rather  than  anaemic  ;  others  are  cyanosed ;  in  some  the  blood- 
counts  are  normal ;  though,  in  a  general  way,  a  contrast  should 
be  drawn  between  the  cyanosis  of  mitral  and  the  pallor  of 
aortic  disease,  A  similar  distinction  holds  good  with  regard 
to  the  expression.  The  cause  of  angina  pectoris  is  sometimes 
cardiac  and  sometimes  aortic,  and  the  frequency  with  which 
disease  of  the  aorta  co-exists  in  aortic  valvular  disease  makes 
the  symptom  of  common  occurrence.  Even  the  throbbing  of 
the  vessels  is  not  pathognomonic,  for  they  throb  whenever  a 
large  quantity  of  blood  is  suddenly  thrown  into  relatively  empty 
vessels ;  and  it  may  be  notable  in  exophthalmic  goitre  and  in 
excited  chlorotic  girls,  quite  apart  from  any  valvular  disease. 

Aortic  Stenosis. — Pure  aortic  stenosis  is  comparatively  un- 
common, and  I  have  only  seen  two  or  three  specimens.  In 
one  case  in  which  the  valve  presented  an  appearance  very 
similar  to  that  shown  in  Fig.  137  a  systolic  murmur  alone  was 
present,  so  that  regurgitation  must  have  been  minimal.  The 
patient,  who  was  aged  sixty- two,  was  admitted  with  oedema, 
Cheyne-Stokes  breathing,  etc.,  and  died  from  progressive 
cardiac  failure.  A  loud,  harsh  murmur  was  audible  all  over 
the  cardiac  area,  replacing  the  first  sound  and  occupying  a 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     347 

considerable  portion  of  the  short  pause.  It  was  loudest  at  the 
aortic  cartilage,  and  the  second  sound  was  inaudible  here;  a  very 
faint  second  sound  could  be  heard  at  the  apex.  The  heart  on 
post-7nortem  examination  was  found  to  weigh  24|^  ounces.  The 
aortic  cusps  were  adherent  to  each  other  for  the  greater  part  of 
their  extent,  and  were  thickly  infiltrated  with  large  calcareous 
masses.  The  lumen  was  greatly  narrowed,  and  the  cusps  were 
practically  immobile,  and  to  the  water-test  notoriously  incom- 
petent, though  no  diastohc  murmur  was  audible  during  life. 

The  a'pex  impulse  is  large  and  heaving  and  well  sustained, 
and  is  displaced  downwards  and  in  lesser  degree  to  the  left. 
A  thrill,  which  is  systoHc  in  rhythm  and  usually  rougher  than 
the  thrill  of  mitral  reflux,  may  be  felt  at  the  base.  The  area 
of  cardiac  dulness  is  increased  downwards  and  to  the  left  in 
corresponding  proportion  to  the  displacement  of  the  apex. 
The  mui'mur  is  diminuendo  and  systohc  in  rhythm,  following 
or  replacing  the  first  sound.  It  is  generally  harsh  and  is  often 
loud,  and  contrasts  with  the  soft  murmur  of  mitral  reflux.  It 
is  heard  best  at  the  aortic  cartilage,  and  is  weU  conducted 
upwards  into  the  neck  along  the  carotid  and  subclavian 
arteries  (Fig.  171).  It  is  sometimes  very  loud,  and  may  be 
audible  on  auscultation  over  the  vertex  of  the  head,  the 
sacrum,  and  the  condyles  of  the  humerus ;  or  even  without 
direct  contact  with  the  patient.  When  heard  at  the  back,  it  is 
loudest  close  to  the  left  border  of  the  vertebral  column,  about 
the  level  of  the  fourth  dorsal  vertebra,  where  the  aorta  first 
comes  into  contact  with  the  spine  (Fig.  172).  The  second 
aortic  sound  ma}'  be  weakened  or  inaudible  if  the  stenosis  is 
considerable  and  the  cusps  stiff.  A  second  sound  is,  however, 
generally  audible  at  the  aortic  cartilage  even  in  well-marked 
cases,  but  is  due  to  the  closure  of  the  pulmonic  valves.  The 
aortic  sound  alone  is  heard  on  auscultation  over  the  carotid 
artery,  and  the  character  of  the  sound  should  be  gauged  only 
b}'  auscultation  above  the  clavicle,  so  as  to  avoid  this  fallacy. 

The  pulse  is  small,  infrequent,  and  slow,  the  wave  rising 
gradually  beneath  the  finger.  It  is  weU  sustained,  and  the 
artery  is  well  fiUed  between  the  beats.  These  characters, 
however,  are  probably  due  to  coincident  arterial  disease  rather 
than  to  the  valvular  defect,  but  the  two  frequently  co-exist ; 


348 


DISEASES  OF  THE  HEART 


an  anacrotic  pulse  is  generally  the  result  of  arterial  hardening, 
just  as  intonation  of  the  second  sound  is  an  indication  of  an 
enlarged  and  stiff  aorta,  rather  than  an  index  of  the  height  of 
the  blood-pressure.  Tracings  show  the  gradual  rise  of  the 
pulse-Avave,  the  rounded  apex,  and  the  gradual  fall ;  the  normal 
Avaves  on  the  downstroke  are  usually  poorly  marked,  and  the 
dicrotic  wave  may  be  wholly  absent. 


Fig.  171. — Diagram  showing  Disteibtj. 
TiON  or  Murmur  of  Aortic  Stenosis. 

y  =  weakening  of  second  aortic  sound. 


Fig.  172. — Diagram  showing  DiSTEiBtr- 
TioN  of  Murmur  of  Aortic  Stenosis. 


Aortic  stenosis  is  compensated  by  hypertrophy  of  the  left 
ventricular  muscle,  and  the  degree  of  the  stenosis  jnsbj  be 
estimated  by  the  degree  of  enlargement,  but  here  again  the 
condition  of  the  arteries  and  kidneys  must  be  taken  into 
account,  for  the  hypertrophy  may  in  large  measure  be  due  to 
arterial  or  renal  disease.  Basal  systolic  murmurs  not  infre- 
quently  obtain  from  mere  roughening   or  hardening   of  the 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     349 


cusps  with  little  or  no  stenosis  ;  the  condition  can  be  recognized 
by  the  absence  of  ventricular  hypertrophy  which  accompanies 
any  definite  narrowing.  The  character  of  the  second  sound  is 
important,  for  its  absence  indicates  gross  valvular  disease. 

The  relationship  between  the  size  and  strength  of  the  pulse 
and  apex  impulse  should  also  be  compared,  for  in  gross  stenosis 
the  pulse-wave  is  small 
and  weak,  while  the  apex 
impulse  is  diffuse  and  well 
sustained. 

A  ortic  Regurgitation .  — 
The  a'pex  impulse  is  power- 
ful, well  sustained,  and 
diffuse,  and  is  displaced 
downwards  and  to  the  left. 
Pulsation  may  be  present 
in  several  interspaces. 
Pulsation,  too,  is  often 
evident  elsewhere ;  towards 
the  base  and  in  the  second 
and  third  right  inter- 
spaces, even  in  the  absence 
of  dilatation,  and  in  the 
carotids  and  above  the 
sternum;  the  whole  chest 
may  heave.  The  head  is 
sometimes  seen   to  shake 

with  each  systole;  and  the   Fig.  173. — Diagbaji  showing  Area  of  Dul- 

,  p     XT        1       J  ^Ess  AND  Pulsation  in  Aortic  Reflux. 

vehemence   of    the    beats 

may  be  so  great  that  they  can  be  felt  by  the  observer  seated 
on  the  bed  without  direct  contact  with  the  patient.  A  th-ill 
can  sometimes  be  felt  over  the  base,  diastoHc  in  rhythm,  and 
succeeding  the  second  sound.  It  is  more  often  absent  than 
present.  The  area  of  cardiac  dulness  is  increased  to  the  left 
and  downwards,  in  corresponding  proportion  to  the  enlarge- 
ment of  the  left  ventricle  (Fig.  173). 

The  murmur  is  diminuendo  and  diastolic  in  rhythm,  succeed- 
ing or  replacing  the  second  sound,  and  running  for  a  variable 
period  into  the  long  pause.     It  is  usually  soft  and  blowing, 


350 


DISEASES  OF  THE  HEART 


and  may  be  distant  and  difficult  to  detect ;  but  it  is  often  loud 
and  superficial;  it  is  sometimes  musical  in  character.  It  is 
heard  best  over  the  sternum,  as  a  rule  with  maximal  intensity 
about  the  middle,  opposite  to  the  third  or  fourth  interspaces ; 
and  is  well  conducted  down  the  sternum  to  the  xiphoid  carti- 
lage, and  in  lessening  degree  to  the  apex  (Fig.  174).  When  it 
is  well  heard  at  the  apex,  it  is  said  (Foster)  to  indicate  a  special 


Fig.  174. — Diagram  showing  Distkibu- 
TioN  OF  Diastolic  Mtjemue  in  Aortic 
Reflux. 

^  =  weakening  of  second  aortic  sound. 


Fig.  175. — Diagram  showing  Area  of 
Diastolic  Mtjrmtjr  of  Aortic  Re- 
flux. 


failure  of  the  left  posterior  cusp.  Sometimes  the  murmur  is 
heard  best  at  the  aortic  cartilage  (Fig.  175),  and  it  may  be 
conducted  into  the  carotids,  but  much  less  frequently  than  the 
systolic  aortic  murmur.  OccasionaUy  it  is  heard  best  towards 
the  xiphoid  end  of  the  sternum.  In  well-marked  cases,  with  a 
loud  murmur,  it  may  be  audible  all  over  the  chest,  and  even 
on  auscultation  over  a  large  artery  hke  the  femoral  in  Hunter's 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     351 

canal.  As  a  rule  this  murmur  of  Duroziez  is  absent,  but  it 
never  occurs  in  the  absence  of  aortic  reflux. 

A  presystoKc  murmur  (Austin  Flint's  murmur)  is  sometimes 
present  at  the  apex  in  these  cases  without  there  being  any 
mitral  disease.  In  the  majority  of  cases,  however,  in  which 
a  presystohc  murmur  is  present  mitral  stenosis  co-exists. 

In  the  majority  of  cases  the  second  aortic  sound  persists  and 
precedes  the  murmur;  but  in  gross  defects,  where  the  cusps  are 
so  shrunken  or  stiffened  that  they  cannot  meet,  the  sound 
may  disappear  and  be  whoUy  replaced  by  the  murmur. 

The  pulse  is  large  and  quick  (shotty,  collapsing,  water- 
hammer,  Corrigan's  pulse),  rapidly  reaching  a  maximum  and 
rapidly  collapsing.  This  character  is  exaggerated  if  the  hand 
is  raised  above  the  head,  and  may  be  better  felt  if  the  forearm 
is  grasped  by  the  whole  hand  than  when  the  artery  alone  is 
felt  by  the  finger.     Capillary  pulsation  is  always  well  marked. 


Fig.  176. — Sphygmogeam  in  Aoktic  REGUBGiTATioir. 


Tracings  show  an  almost  vertical  abrupt  upstroke,  a  pointed 
apex,  and  a  sudden  fall,  the  aortic  notch  being  low  down  and 
the  dicrotic  wave  poorly  developed  (Fig.  176). 

Aortic  regurgitation  is  compensated  by  enlargement  and 
hypertrophy  of  the  left  ventricle,  and  the  degree  of  the  reflux 
may  be  estimated  by  the  degree  of  the  enlargement.  Mere 
hypertrophy  of  the  ventricular  waU  is  insufficient,  the  ven- 
tricular content  must  be  larger;  for  if  the  aortic  content  during 
diastole  is  to  remain  of  normal  amount,  the  systohc  influx 
must  be  abnormally  large  to  compensate  the  amount  lost  hy 
regurgitation.  In  the  same  way  the  pulse-pressure  is  an  index 
of  the  degree  of  the  fault,  for  the  systohc  pressure  must  be 
abnormally  high,  if,  notwithstanding  the  rapid  fall  of  pressure 
during  diastole,  the  mean  aortic  pressure  is  to  remain  normal. 
The  pulse-pressure  is  often  a  valuable  guide  in  these  cases,  for 
it  is  related  to  aortic  reflux  alone.     Not  infrequently  mitral 


352  DISEASES  OF  THE  HEART 

and  aortic  reflux  co-exist,  and  the  enlargement  of  the  left 
ventricle  is  due  to  the  two  causes  combined;  and  it  is  difficult 
in  other  wa^'s  to  assess  the  proper  value  of  each  individual 
defect.  The  point  may  be  determined  by  the  finger,  for  the 
pulse  is  more  collapsing  and  "  quicker,"  the  greater  the  reflux. 

The  pulse-pressure,  however,  is  only  useful  as  a  gauge  of 
the  degree  of  the  leak  when  compensation  is  eftective.  Two  of 
my  patients  had  blood-pressures  which  were  similar  (115-92 
mm.  Hg),  but  the  lesions  were  in  no  way  comparable.  In 
one  there  was  no  evidence  of  cardiac  weakness,  the  patient 
being  under  observation  on  account  of  an  attack  of  acute 
rheumatism,  and  the  lesion  was  minimal.  The  other  patient 
was  moribund  at  the  time,  fainting  habitually  when  at  stool, 
and  sometimes  when  he  merely  sat  up  in  bed.  Muscular 
weakness  was  so  extreme  that  the  pulse-pressure  could  not  be 
raised  to  a  satisfactory-  level,  the  lesion  being  gross .  Coincident 
stenosis  may  whollj^  alter  the  characteristic  pulse  of  regurgita- 
tion if  the  obstruction  is  considerable  and  the  outflow  of  blood 
gradual  and  prolonged. 

Weakening  or  disappearance  of  the  second  aortic  sound  is 
also  an  important  guide  to  the  grade  of  the  lesion,  for  the 
presence  of  a  norma]  sound  indicates  that  the  valves  are 
fulfilHng  their  purpose  fairly  well,  notwithstanding  the  leak. 
This  may  be  seen  in  tracings ;  a  well-marked  dicrotic  wave  has 
a  similar  significance.  The  length  of  the  murmur  is  an  indi- 
cation of  the  duration  of  the  regurgitation.  In  shght  cases 
it  mereh'  follows  the  second  sound  for  a  short  distance,  but 
in  severe  leaks  may  occupy  the  whole  of  diastole. 

The  Physical  Signs  o!  Valvular  Disease  of  the  Right  Heart. 

— Valvular  disease  on  the  right  side  of  the  heart  is  uncommon. 
Both  the  pulmonary  and  the  tricuspid  valves  maj-  be  affected 
bj'  acute  endocarditis,  but  this  is  generaU}'  malignant  in 
tj-pe  and  secondary  to  septic  foci  elsewhere,  the  organisms 
being  conveyed  directly  to  the  heart  through  the  veins;  and  is 
rarely  of  the  simple  form,  so  that  chronic  lesions  are  unusual. 
When  chronic  lesions  occur,  they  are  almost  alwaj's  accom- 
panied by  disease  of  the  mitral  or  aortic  valves,  of  older  date 
and  more  extreme  grade.  The  tricuspid  valve  is  affected 
much  more  frequently  than  the  pulmonary. 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     353 

Congenital  defects  are  fairly  common,  and  affect  the  pul- 
monary artery  in  particular,  tricuspid  lesions,  like  those  of 
the  mitral  valve,  being  extremely  rare.  As  pulmonary  defects 
arise  during  the  development  of  the  septum  of  the  truncus 
arteriosus,  the  aortic  valve  is  also  frequently  involved. 

Functional  (secondary)  incompetence  of  the  tricuspid  valve, 
on  the  other  hand,  is  of  common  occurrence.  The  tricuspid 
is  similar  in  its  structure  to  the  mitral  valve,  and  becomes 
incompetent  if  the  right  ventricle  dilates,  the  muscular 
sphincter  becoming  unable  to  narrow  the  orifice  sufficiently 
for  the  cusps  to  occlude  it.  The  right  ventricle  is  always  over- 
worked in  mitral  disease  and  in  chronic  pulmonary  diseases, 
such  as  emphysema  and  fibroid  phthisis,  and  although  com- 
pensatory hypertrophy  ensues  and  so  allows  the  work  to  be 
carried  on  for  a  time,  it  ultimately  becomes  insufficient,  and 
the  ventricle  gives  way  beneath  the  strain.  In  acute  pul- 
monary disease  a  temporary  incompetence  is  not  unusual. 

Tricuspid  incompetence,  even  when  due  to  muscular  weak- 
ness, is  always  extremely  serious,  for  the  strain  is  thrown 
upon  the  right  auricle,  which  is  incapable  of  satisfactory 
compensatory  hypertrophy,  so  that  venous  stasis  follows. 
The  appearance  of  oedema  in  the  feet  and  passive  venous 
congestion  of  the  hver  are  the  result. 

Pulmonary  incompetence  may  own  a  similar  cause.  In 
cases  of  extreme  mitral  stenosis  the  blood-pressure  in  the 
pulmonary  circuit  is  extremely  high,  and  the  artery  may 
dilate  and  incompetence  ensue  without  any  lesion  of  the  cusps. 
With  improvement  the  characteristic  murmur  may  disappear. 
The  comparable  incompetence  in  cases  of  high  aortic  blood- 
pressure  is  rare,  for  the  aorta  is  thicker  than  the  pulmonary 
artery,  and  its  valves  remain  competent  (in  experiment) 
under  a  pressure  which  produces  notable  regurgitation  at 
the  pulmonary  valve  (G.  A.  Gibson). 

Tricuspid  incompetence  is  probably  the  most  frequent  as 
well  as  the  most  serious  valvular  lesion,  for  it  occurs  in  many 
diseases  as  a  sequel  of  cardiac  failure,  and  so  is  the  immediate 
precursor  of  death. 

Pulmonary  Stenosis. — The  murmur  is  usually  loud  and  harsh 
and  superficial,  and  replaces  or  follows  the  first  sound.     It 

23 


354  DISEASES  OF  THE  HEART 

is  heard  best  in  the  second  left  interspace  close  to  the  sternum, 
and  is  well  conducted  to  the  left  clavicle  (Fig.  177).  It  is 
not  conducted  into  the  carotid  artery.  The  maximum  in- 
tensity at  the  back  is  some  distance  away  from  the  spine, 
about  the  centre  of  the  left  scapula.  The  second  pulmonic 
sound  is  weakened  or  absent.  A  thrill  which  is  systolic  in 
rhythm  is  generally  present,  with  maximum  intensity  in  the 
second  left  interspace.  The  right  heart  is  hypertrophied, 
and  pulsation  may  be  evident  in  the  epigastrium,  at  the  xiphoid 
end  of  the  sternum,  and  in  the  fourth  and  fifth  right  inter- 
spaces. 

Compensation  is  effected  hj  hypertrophy  of  the  right 
ventricle,  but  its  degree  is  difficult  to  gauge;  but  the  Iwper- 
trophy  is  considerable,  and  the  stenosis  is  great  if  the  lower 
end  of  the  sternum  pulsates.  The  duration  of  the  murmur 
is  an  important  guide  to  the  grade  of  the  defect.  Absence  of 
the  second  sound  indicates  a  gross  lesion  of  the  valve. 

Pulmonary  Regurgitation. — The  murmur  is  usually  soft  and 
blowing  in  character,  and  is  diastolic  in  rhythm,  replacing  or 
following  the  second  sound.  It  is  heard  best  in  the  second 
or  third  left  interspaces  close  beside  the  sternum,  and  is  con- 
ducted downwards,  and  in  the  direction  of  the  xiphoid  car- 
tilage (Fig.  178).  The  second  'pulmonic  sound  may  be  weakened 
or  absent.  A  soft  diastolic  thrill  may  be  felt  to  the  left  of 
the  sternum.  The  right  heart  is  hypertrophied,  and  pulsation 
may  be  present  in  the  epigastrium,  at  the  xiphoid  end  of  the 
sternum  and  in  the  fourth  and  fifth  right  interspaces . 

The  distribution  of  the  murmur,  if  it  is  loud,  thus  closely 
resembles  that  of  the  murmur  of  aortic  regurgitation.  The 
important  differences  are  the  enlargement  of  the  right  heart, 
the  interference  with  the  pulmonic  second  sound,  and  the 
absence  of  the  characteristic  pulse  of  aortic  disease. 

Compensation  is  effected  by  hypertrophy  of  the  right  ven- 
tricle, but  its  degree  is  difficult  to  gauge.  If  the  lower  end 
of  the  sternum  pulsates,  the  hypertrophy  is  considerable  and 
the  reflux  is  great.  Absence  of  the  second  sound  indicates 
a  gross  lesion  of  the  valve. 

Tricuspid  Regurgitation. — Pulsation  is  generally  evident  at 
the  lower  end  of  the  sternum  and  in  the  epigastrium,  and  often 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     355 

in  the  fourth  and  fifth  right  interspaces.  The  apex  impulse 
IS  not  displaced,  but  it  may  be  impalpable.  A  thrill  is  rarely 
present.  The  area  of  dulness  is  increased  to  the  right,  but 
does  not  trespass  upwards  above  the  third  costal  cartilage 
(Fig.  167).  The  murmur  is  systohc  in  rhythm,  and  replaces 
or  succeeds  the  first  sound;  it  is  usually  soft  and  blowing  in 
character,  is  heard  best  at  the  xiphoid  end  of  the  sternum 


Fig.  177. — Diagram  showing  the  Dis- 
tribution OF  THE  Systolic  Murmur 
OF  Pulmonary  Stenosis. 


Fig.  178. — Diagram  showing  Distri- 
bution OF  Diastolic  Murmur  of 
Pulmonary  Reflux. 


and  is  well  conducted  towards  the  right  nipple 
At  the  back  its  maximum  intensity  is  at  the  an 
right    scapula.       The   second   pulmonic    sound   is 
The  jugular  veins  are  usually  greatly   distended, 
pulsate  forcibly.       The   hver,    too,  may  show   an 
pulsation,   and  is  generally  notably  enlarged  and 
palpation. 

Tricuspid  regurgitation  is  compensated  to  some 


(Fig.  179). 

gle  of  the 

weakened, 
and  may 
expansile 

tender  on 

extent  by 


356  DISEASES  OF  THE  HEART 

dilatation  of  the  right  ventricle  and  hypertrophy  of  its  wall, 
and  by  dilatation  and  hypertrophy  of  the  right  auricle.  The 
results  are,  however,  less  satisfactory  than  in  mitral  regurgi- 
tation, for  failure  of  the  right  auricle  entails  general  venous 
stasis,  as  it  has  no  assistance,  when  in  difficulty,  that  can  be 
compared  to  the  action  of  the  right  ventricle  in  failure  of  the 
left  auricle.  The  degree  of  auricular  distension  may  be 
measured  by  the  increase  in  the  size  of  the  cardiac  dulness 
to  the  right,  or  by  the  size  of  the  distended  veins  and  the  con- 
gested liver  and  the  amount  of  oedema.  If  the  liver  is  cir- 
rhotic, however,  the  enlargement  is  rarely  great.  The  char- 
acter of  the  cervical  pulse  is  of  help,  for  in  free  tricuspid 
regurgitation  the  auricle  is  rapidly  distended  by  the  reflux 
from  the  ventricle,  and  the  v  wave  occurs  prematurely,  and 
is  merged  into  the  carotid  wave,  the  x  depression  being  lost 
(c/.  Fig.  60,  p.  107). 

Tricuspid  Stenosis. — The  murmur  is  diastolic  (presystohc) 
in  rhythm  and  crescendo  and  rough  in  character,  but 
is  rarely  as  loud  as  the  corresponding  murmur  of  mitral 
stenosis.  It  is  heard  best  at  the  xiphoid  end  of  the  sternum, 
and  is  of  limited  distribution  (Fig.  180).  A  rough  presystolic 
thrill  has  been  observed  in  the  same  situation. 

Tricuspid  stenosis  is  usually  associated  with  other  valvular 
defects,  and  often  with  mitral  stenosis.  In  some  of  these  cases 
two  maxima  of  the  murmur  have  been  observed — in  the 
apical  region  and  at  the  xiphoid  end  of  the  sternum — but 
the  two  murmurs  are  often  indistinguishable.  It  must  be 
remembered  that,  in  cases  where  the  left  heart  is  hyper- 
trophied,  the  presystolic  murmur  of  mitral  stenosis  may  be 
well  heard  even  over  the  sternum,  and  its  thrill  may  be  felt 
in  the  epigastrium. 

Tricuspid  stenosis  is  compensated  by  hypertrophy  of  the 
right  auricle,  which  is  rarely  sufficient . 

The    Physical    Signs    in    Congenital    Valvular    Disease. — The 

murmurs  which  occur  in  congenital  heart  disease  are  very 
perplexing,  for  the  defects  are  frequently  multiple,  and  an 
accurate  diagnosis  is  usually  only  possible  on  post-mortem 
examination.  In  cases,  however,  where  there  is  a  defect  in 
the  interventricular  septum,  and  in  those  with  a  persistent 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     357 


ductus    arteriosus,    the    lesions    may    manifest    characteristic 
murmurs . 

The  murmur  which  is  present  in  defect  of  the  interventricular 
septum  (bruit  de  Roger)  is  usually  loud  and  harsh;  it  com- 
mences early  in  systole,  and  is  prolonged  into  diastole,  so  that 
it  hides  or  covers  the  second  sound,  which  may,  however, 
be  distinctly  heard  at  the  base.     The  murmur  has  its  site  of 


Fig.  179. — Diagkam  showing  Distribu- 
tion OP  Systolic  Mukmue  of  Tri- 
cuspid Eeflux. 


Fig.  180. — Diagrasi  showing  Distri- 
BTJTioN  OF  Presystolic  Murmur  of 
Tricuspid  Stenosis.? 


maximum  intensity  at  the  left  side  of  the  sternum  close  to 
the  xiphoid,  and  is  not  well  conducted  into  the  carotid  artery 
or  into  the  axilla.* 

The  murmur  in  patent  ductus  arteriosus  is  also  long,  and 
occupies  both  systole  and  diastole.  It  is  usually  loud  and 
harsh,  replacing  or  running  out  of  the  first  sound,  and  per- 
sisting for  a  variable  period  into  the  long  pause,  sometimes 

*  Cowan  and  L.  Storey,  Glasgoiv  Med.  Journ.,  1909,  vol.  Ixxii.,  p.  425. 


358 


DISEASES  OF  THE  HEART 


even  up  to  the  commencement  of  the  succeeding  first  sound. 
It  is  usually  loudest  at  its  commencement  and  diminuendo, 
but  it  may  wax  about  its  middle  and  then  wane.  The  second 
sound  may  be  distinctly  audible.  The  murmur  is  usually 
heard  best  in  the  second  left  intercostal  space,  about  2  inches 
from  the  sternum,  where  a  thrill  can  generally  be  felt  with  the 
hand.  The  murmur  is  well  conducted  to  the  left  clavicle 
(Fig.  181);  but  it  may  be  heard  best  at  the  back  over  the  left 

scapula.  This  variation  in 
distribution  is  due  to  varia- 
tions in  the  other  defects. 
The  ductus  persists  when 
the  pulmonary  artery  is 
stenosed  at  its  orifice,  so 
that  the  pulmonary 
branches  may  be  supplied 
from  the  aorta ;  but  it  may 
also  persist  if  the  aortic 
orifice  is  narrowed,  so  that 
the  descending  aorta  may 
be  filled  from  the  pul- 
monary artery.  In  some 
cases,  then,  the  flow  of 
blood  is  from  aorta  to 
pulmonary  artery;  in 
others,  from  pulmonar}^ 
artery  to  aorta.  In  many 
cases  aortic  or  pulmonary 

Fig.  181. — Diagkam  showing  Disteibution  stenosis    gives    a    special 
OF  Mtjemur  of  Patent  Ductus  Arteki-  ,       .         .  ,  •      i 

osus,  emphasis    at   a  particular 

The  distribution  of  the  murmur  in  this  case      site  to  the  first  portion  of 
IS  unusual.  themurmur.    The  murmur 

which  is  best  heard  at  the  back  of  the  chest  is  probably  that 
which  is  produced  by  blood  flowing  from  pulmonary  artery 
into  aorta,  the  vibrations  being  loudest  where  the  junction 
of  the  blood  currents  is  nearest  to  the  surface. 

The  murmurs  in  these  two  defects  resemble  each  other  in 
one  respect — namely,  that  they  occupy  both  systole  and 
diastole  without  any  interval  between  the  systolic  and  the 


DIAGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     359 

diastolic  portions.  Such  murmurs  cannot  originate  at  any  of 
the  valves,  and  only  obtain  when  a  communication  exists 
between  separate  cavities  or  vessels.  These  murmurs  are  not 
confined   to   congenital   defects,    and   may   be   met   with    in 


Fig.  182. — Stenosis  of  Left  Pulmonary  Arteey  from  Pkessuee  of  a 
Malignant  Growth  {a). 

aneurismal  varix  as  weU  as  in  cases  of  ulcerative  endocarditis 
or  aneurism,  if  rupture  takes  place  into  adjacent  cavities  or 
vessels. 

The  distribution  of  murmurs  produced  at  the  valves  is  a 


360 


DISEASES  OF  THE  HEART 


natural  sequel  to  their  anatomical  position  within  the  chest. 
Any  abnormality  in  distribution  indicates  that  some  abnormal 
factor  has  come  into  action.  In  a  case  of  multiple  cutaneous 
cancer,  for  instance,  a  secondary  growth  occurred  in  the 
mediastinum,  and  nipped  the  left  pulmonary  artery  just  after 
the  bifurcation  (Fig.  182),  and  a  loud  systohc  murmur  made 


Fig.  183. — Diagram  showing  Distbi- 
BXJTION  OF  Systolic  Mubmur. 


Fig. 


its  appearance.     It  was  well  heard 
but  it  was  louder  beneath  the  left 
the  left  scapula   (Figs.    183,    184), 
stenosis  was  situated  some  distance 
valve  and  the  front  of  the  chest, 
an    intrathoracic    tumour,    or    a 
may  also  lead  to  the  conduction 
directions. 


184. — DiAGRAJVI    SHOWING    DISTRIBU- 
TION OF  ISystolic  Murmur. 

at  the  second  left  space, 
clavicle,  and  loudest  over 
clearly  showing  that  the 
away  from  the  pulmonary 
An  aneurismal  dilatation, 
pulmonary  consohdation, 
of  murmurs  in  abnormal 


CHAPTER  XXV 
THE  PROGNOSIS  OF  CHRONIC  VALVULAR  DISEASE 

The  difficulty  of  forming  an  accurate  prognosis  in  disease  of 
the  heart  has  recently  been  emphasized  by  Sir  Chfford  Allbutt, 
in  a  lecture  to  the  Chelsea  Chnical  Society;  but  though  no  one 
denies  the  frequency  of  error,  his  opinion  is  probably  too 
gloomy,  and  a  fairly  accurate  forecast  can  generally  be  made 
if  all  the  facts  of  the  case  are  carefully  scrutinized.  A  wide 
outlook,  however,  is  necessary,  as  the  cardiac  symptoms  and 
signs  are  by  no  means  the  most  important  elements.  An 
accurate  prognosis,  too,  requires  repeated  and  continuous  ob- 
servation, and  can  rarely  be  made  on  an  isolated  examination. 

In  the  presence  of  active  symptoms  their  progress  from  day 
to  day  forms,  of  necessity,  the  main  basis  on  which  an  opinion 
can  be  formed.  The  size,  the  strength  and  rate  of  the  pulse, 
the  degree  of  oedema  and  hepatic  enlargement,  the  frequency 
of  the  respirations,  and  the  grade  of  the  dyspnoea  or  orthopnoea, 
the  pallor  or  the  cyanosis,  the  amount  of  urine  excreted,  the 
discomfort,  the  restlessness  and  the  amount  of  sleep  obtained, 
have  all  to  be  accurately  recorded  and  compared  from  day  to 
day.  And  it  must  ever  be  remembered  that  the  "  accidents  "  of 
valvular  disease,  produced  by  embolism,  occur  most  frequently 
in  the  presence  of  general  symptoms  of  cardiac  distress,  and 
may,  in  a  moment,  alter  the  whole  aspect  of  affairs.  But  em- 
bohsm  is  by  no  means  invariably  fatal,  and  I  have  seen  patients 
hve  in  comfort  for  several  years  after  the  occurrence  of  a 
■cerebral  embohsm  or  a  pulmonary  infarct,  though  this  is 
certainly  unusual. 

In  exceptional  cases,  too,  recovery  may  ensue  after  serious 
embohc  phenomena.  A  woman,  aged  forty,  was  recently  in 
my  wards  suffering  from  cardiac  failure  consequent  on  mitral 
disease  and  auricular  fibrillation.     Four  and  a  half  years  pre- 

361 


362  DISEASES  OF  THE  HEART 

viously  the  right  hand  had  suddenly  become  painful  and  cold  and 
powerless,  and  gangrene  followed,  which  necessitated  amputa- 
tion through  the  forearm .  The  radial  and  brachial  pulses  could 
not  be  felt  before  operation,  though  the  subclavian  artery  was 
pulsating,  and  the  condition  was  apparently  the  result  of  an 
embohc  block  associated  with  organic  mitral  disease  of  rheu- 
matic origin.  She  was  able  to  perform  her  household  duties  until 
a  few  months  before  her  second  admission  into  hospital. 

Of  isolated  sj-mptoms,  two  are  particularly  important  and 
of  evil  omen.  Few  patients  recover  who  display  distinct  jaun- 
dice with  an  enlarged,  congested  liver,  or  who  lie  in  the  trough 
of  the  bed,  with  lack-lustre  ej^es,  completely  indifferent  tO' 
their  surroundings. 

Sir  William  Brcaclbent  laid  down  a  useful  scheme  of  inquiry 
on  which  the  prognosis  should  be  based  in  those  cases  in  whom 
the  urgencj"  of  the  symptoms  is  not  immediate.  To  this  I 
have  made  some  additions.  The  nature,  the  site,  and  the- 
grade  of  the  lesion ;  the  rhythm  of  the  heart ;  the  presence  or 
absence  of  associated  disease  in  other  viscera ;  the  degree  to 
which  compensation  has  been  eft'ected  ;  the  cause  of  the  failure 
which  has  brought  the  patient  under  observation — have  all  to 
be  taken  into  account,  as  weU  as  the  age  and  sex  of  the  patient 
and  his  social  circumstances  and  habits. 

1.  The  Nature  of  the  Lesion. — The  most  favourable  cases  are 
those  in  which  the  mitral  valve  has  become  incompetent  as 
the  result  of  anaemia  or  debility,  if  the  cause  can  be  removed 
and  its  recurrence  prevented.  The  corresponding  incompe- 
tence of  the  tricuspid  valve  is  more  serious,  for  it  rarely  pro- 
duces symptoms  in  the  absence  of  organic  disease  of  the  lungs 
or  left  heart,  and  the  cause  of  its  occurrence  consequently 
persists.  A  congenital  defect  is  not  progressive,  but  the 
majority  of  patients  die  in  early  life  in  consequence  of  the 
disturbance  of  the  circulation,  or,  if  they  survive,  are  essentially 
weakhngs;  and  valves  which  are  so  deformed  are  pecuharly 
prone  to  be  affected  by  acute  inflammatory  processes.  In 
patients,  however,  who  have  reached  maturity  with  good 
physique  and  nutrition,  and  absence  of  any  evidence  of  cardiac 
distress,  the  outlook  is  favourable,  but  though  many  cases 
have  been  recorded  who  lived  to  thirty  and  forty  years  of  age^ 


PROGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     363 

the  records  are  less  numerous  in  the  fifties,  and  I  can  find  but 
few  over  sixty.  Of  my  own  cases,  onlj  two  have  as  yet 
reached  forty. 

A  chronic  valvular  lesion  due  to  a  long  antecedent  rheumatic 
infection  is  unhkely  to  be  progressive  unless  the  exciting  cause 
recurs,  and  has,  in  consequence,  a  good  prognosis ;  but  the  age 
of  the  patient  must  be  taken  into  account,  for  rheumatism 
often  recurs  in  the  teens  and  twenties,  though  less  frequently 
after  thirty.  A  syphilitic  lesion  may  become  stationary  if  it 
is  recognized  and  treated.  The  progressive  lesions  are  un- 
favourable. Acute  endocarditis  can  only  be  gauged  by  the 
progress  of  the  case  and  the  degree  of  the  compensatory 
changes  in  the  size  of  the  chambers.  The  occurrence  of  symp- 
toms of  cardiac  failure  is  always  a  serious  sign,  particularly  if 
they  obtain  during  the  febrile  stage.  The  degenerative  chronic 
lesions  are  necessarily  progressive,  though  the  rate  of  progress 
varies  in  different  cases.  Patients  rarely  live  for  five  years 
after  symptoms  have  once  made  their  appearance. 

2.  The  Site  of  the  Lesion. — The  possibility  of  sudden  death 
in  patients  who  are  the  subject  of  valvular  disease  has  rarely 
to  be  considered,  so  long  as  the  patient  is  not  confined  to  bed, 
though  it  is  by  no  means  uncommon  in  cases  where  serious 
sj^mptoms  are  already  present.  Sudden  death,  according  to 
Kisch,  is  uncommon  before  the  age  of  thirty,  and  is  most  frequent 
between  fifty  and  sixty.  It  is  apt  to  occur  in  fat  people  with 
general  arterio-sclerosis,  and  in  patients  with  f  att}^  dilated  hearts 
and  mitral  or  aortic  insufficiency.  It  is  not  uncommon  in  aortic 
aneurism,  in  cases  with  irregular  or  infrequent  pulses,  in  fat 
persons  who  suffer  from  angina,  and  in  emphysematous  patients 
who  have  manifested  symptoms  of  cardiac  weakness.* 

The  causes  of  sudden  death  are  thus  related  to  myocardial 
rather  than  to  valvular  lesions,  and  are  often  the  result  of 
coronarj^  disease.  I  have  notes  of  6  cases  in  which  death 
ensued  without  warning,  and  in  4  the  heart  was  ruptured.  In 
the  other  2  the  coronary  arteries  were  blocked  by  emboh,  which 
were  derived  in  1  case  from  the  apex  of  a  dilated  left  ventricle, 
and  in  the  other  from  f ungating  vegetations  upon  the  valves. 

*  It  has  been  suggested  that  the  occurrence  of  ventricular  fibrillation  may- 
be the  cause  of  sudden  death  in  cases  where  the  auricles  are  fibrillating.  In 
experiment  such  a  sequel  is  not  uncommon. 


364  DISEASES  OF  THE  HEART 

Of  the  valvular  lesions,  aortic  regurgitation  is  that  which 
most  often  ends  suddenly.  The  strain  upon  the  left  ventricle 
is  great  if  the  regurgitation  is  extreme  and  occurs  during 
diastole,  when  the  ventricle  is  "defenceless,"  as  it  is  not  in 
contraction,  and  a  fatal  syncope  may,  in  consequence,  occur. 
In  aortic  disease,  too,  the  coronary  arteries  are  more  fre- 
quently damaged  than  in  mitral  disease,  and  the  muscle  is 
thus  more  likely  to  be  abnormal.  In  mitral  stenosis  embohsm 
is  relatively  frequent,  and  may  occasion  sudden  death.  The 
experience  at  St.  Mary's  Hospital  may  be  quoted:  4  out  of 
38  cases  of  aortic  regurgitation  died  suddenly,  but  only  1  of 
53  cases  of  mitral  stenosis,  and  2  of  44  cases  of  mitral  reflux, 
and  in  the  latter  serious  sj^mptoms  were  already  present.  In 
aortic  stenosis  (11  cases)  there  were  no  sudden  deaths. 

The  most  serious  valvular  lesion  is  disease  of  the  tricuspid 
valve.  It  is  uncommon  unless  in  the  form  of  "functional" 
insufficiency,  secondary  to  left-sided  disease,  or  affections  of 
the  lung,  but  as  compensation  has  to  be  effected  by  the  right 
auricle,  its  degree  is  usually  insufficient,  and  it  is  rarely 
maintained  for  any  length  of  time.  Tricuspid  regurgitation, 
aortic  regurgitation,  mitral  stenosis,  aortic  stenosis,  mitral 
regurgitation,  in  order,  probably  represents  fairly  accurately 
the  relative  danger  of  the  lesions . 

It  is  impossible  to  give  figures,  for  the  lesions  are  rarely 
comparable;  for  example,  the  age  at  death  in  mitral  disease 
following  acute  rheumatism  in  early  life  cannot  be  contrasted 
with  the  age  at  death  in  mitral  disease  the  result  of  chronic 
endocarditis  which  ensued  after  fiftj-.  Balfour's  case,  where 
the  patient  had  mitral  reflux  for  sixty-six  years,  had  the 
longest  duration  which  I  can  find  recorded. 

3.  The  estimation  of  the  degree  of  the  lesion  has  already 
been  considered. 

4.  The  Rhythm  of  the  Heart. — I  had  hoped  to  have  been  able 
to  give  definite  figures  as  to  the  frequency  with  which  irregu- 
larities occur  in  mitral  and  aortic  disease  in  the  presence  of 
symptoms,  but  my  records  are  stiU  scanty.  In  the  mitral  series 
(102  cases),  auricular  fibrillation  occurred  in  19  cases,  paroxys- 
mal tachycardia  in  5,  extra-systoles  in  2,  and  heart-block,  nodal 
rhj^thm,  and  an  undecipherable  irregularity  in  1.  In  the  aortic 
series  (58  cases),  extra-systoles  occurred  in  9,  auricular  fibril- 


PROGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     365 


lation  in  2,  paroxj^smal  tachycardia  in  1,  and  nodal  rhythm 
in  3.  But  the  records  are  imperfect,  and  irregularities 
were  more  frequent  than  the  figures  suggest,  though  the  large 
majority  of  patients  had  a  regular  pulse.  Death  may  occur, 
in  mitral  stenosis,  without  any  alteration  in  the  rhythm, 
even  in  cases  where  the  valvular  lesion  is  considerable  and  of 
old  standing.  A  woman  who  was  under  my  charge  when 
house  physician  in  1895  in  Dr.  Tennent's  wards  was  admitted 
into  my  wards  in  1912  for  a  few  weeks  before  her  death,  at  the 
age  of  forty-four.  The  mitral  lesion  had  existed  for  seventeen 
3^ears  at  least,  and  probably  for  longer,  and  the  right  heart  was 
permanently  enlarged ;  but  not\^'ithstanding  the  repeated  occur- 
rence of  pulmonary  infarcts,  the  cardiac  rhythm  remainedregular, 
and  the  auricular  wave  persisted  in  the  cervical  curve. 

The  prognosis  in  cases  with  a  regular  cardiac  rhythm  is 
apparently  less  serious  than  in  those  with  an  irregular  rhythm. 
But  the  other  factors  must  be  comparable  if  the  comparison  is 
to  be  exact,  and  as  a  permanently  irregular  rhythm  is  generally 
due  to  myocardial  changes,  the  difference  may  be  merely  due 
to  the  greater  incidence  of  the  latter.  From  the  practical 
point  of  view,  however,  the  distinction  is  important.* 


i 

All  Cases.     1      "l^ytbm            Rhythm 

Regiiiar.           IiTegular.     j 

1 
jVIitral  disease 

Death  in  . . 

Per  cent.  . . 
Aortic  disease 

Death  in  . . 

Per  cent.  . . 

102                   73 
32                   15 
31-4               20-5 
58                   43 
17                   11 
29-3               25-6 

29 
17 
58-6 
15 
6 
40 

1 

Mitral  Disease.      Aortic  Disease. 

Auricular  fibrillation 

Death  in  . . 
Extra-systoles 

Death  in  . . 
Paroxysmal  tachycardia     . . 

Death  in  . . 
Heart-block  . . 

Death  in  . . 
Xodal  rhythm 

Death  in    . . 

19                         2 
11                        — 

2                         9 

2                        2 

5           i             1            i 
2                         1 
1                      — 

■        ■                   i 

D.  MacDonald. 


366  DISEASES  OF  THE  HEART 

5.  The  PreseThce  of  Disease  in  Other  Viscera. — I  have  already 
indicated  the  frequency  with  which  cardiac  valvular  disease 
is  associated  with  lesions  in  other  viscera,  the  lungs,  the 
arteries,  and  the  kidneys  being  most  often  involved.  The 
presence  of  other  lesions  always  intensifies  the  gravity  of  the 
prognosis.  In  young  people  the}^  occur  as  a  result  of  the 
cardiac  lesion  or  irrespective  of  it,  but  in  elderly  persons 
they  are  frequently  the  cause  of  the  valvular  disease,  and  the 
recognition  of  the  cardiac  element  alone  leads  to  an  erroneous 
idea  of  the  case;  for  in  many  patients  the  cardiac  flaw  is 
immaterial,  and  the  progress  is  dependent  upon,  and  the 
symptoms  are  due  to,  the  other  lesions.  In  comparable  cases, 
of  course,  the  prognosis  is  better  in  the  purely  cardiac  group. 
Patients  with  cardiac  disease  and  hepatic  cirrhosis  rarely  live 
long  after  the  latter  has  been  recognized.  Notable  emacia- 
tion is  always  of  serious  import. 

6.  The  Degree  of  Compensation. — James  Mackenzie  has 
recently  emphasized  the  well-known,  but  oft-forgotten, 
aphorism  that  the  integrity  of  the  cardiac  muscle  is  the  most 
important  factor  in  valvular  disease,  and  that,  so  long  as  the 
cardiac  work  is  carried  on  easily,  the  exact  degree  or  nature 
of  the  valvular  flaw  is  immaterial — in  short,  that  "the  proof 
of  the  pudding  is  in  the  eating."  With  this  everyone  will 
agree,  and  so  long  as  the  ordinary  business  of  life  is  conducted, 
without  discomfort,  the  immediate  outlook  is  satisfactory. 

It  is  difiicult  to  estimate  the  reserve  power  of  the  heart, 
and  it  can  only  be  gauged  by  repeated  experiment  as  to  the 
amount  of  physical  exertion  which  can  be  undergone  without 
discomfort.  Even  here  a  fallacy  is  at  once  apparent,  for 
air~of~us  who  -have  entered  or  passed  the  forties — the  forties 
which  are  so  often  as  stormy  in  life  as  thej^  are  at  sea — are 
well  aware  of  the  necessitj^  of  taking  things  quietly  at  the  com- 
mencement of  our  annual  holiday,  and  that  an  amount  of 
exertion  which  can  be  indulged  in  with  impunity,  or  even  with 
benefit,  towards  its  conclusion  may  be  badly  borne  at  its 
commencement . 

"^In  a  general  way  a  conclusion  may  be  reached.  If  a  day's 
goK  or  shooting  is  not  accompanied  by  undue  weariness  or 
breathlessness,    if    business    activities    entail   no   special   dis- 


PROGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     367 

ability,  and  if  a  hill  can  be  surmounted  mtH  ease,  the  cardiac 
reserve  is  ample,  and  little  apprehension  need  be  felt.  Con- 
Tersely,  if  a  slow  walk  on  the  flat  is  the  only  comfortable 
mode  of  progression,  if  CBdema  appears  in  the  ankles  at  night, 
and  if  breathlessness  ensues  on  walking  upstairs,  the  reserve 
is  shght,  and  immediate  trouble  may  be  anticipated.  In 
the  consulting-room  similar  experiments  may  be  tried,  and 
the  results  of  hopping  round  the  room  or  walking  upstairs 
may  be  investigated.  The  behaviour  of  the  pulse  on  exertion 
is  often  a  useful  guide.  Its  rate,  when  the  patient  is  re- 
cumbent, is  normally  some  seven  to  fifteen  beats  less  than 
when  he  is  standing  up.  In  the  milder  forms  of  insufficiency 
the  difference  is  greater,  or  no  fall  in  rate  ensues  when  he  hes 
down.  On  exertion,  in  healthy  individuals,  the  pulse-rate  at 
first  increases,  but  rapidly  regains  its  former  rate  when  the 
patient  is  again  seated.  The  majority  of  normal  persons 
regain  their  usual  pulse-rate  A^dthin  a  couple  of  minutes  after 
walking  upstairs,  but  in  myocardial  insufficiency  the  period 
may  be  delayed  for  four  or  ten,  or  even  thirtj",  minutes.  In 
exceptional  cases  the  pulse-rate  may  be  slowed  by  exercise. 
This  is  generall}^  due  to  some  of  the  beats  becoming  imper- 
ceptible to  the  finger,  though  it  is  said  to  result  in  exceptional 
instances  from  true  slowing  of  the  ventricular  contractions. 
The  occurrence  is,  in  any  case,  a  sign  of  evil  significance. 

7.  The  Cause  of  Failure. — In  patients  who  come  under 
observation  on  account  of  symptoms  of  cardiac  weakness, 
the  precise  cause  of  the  failure  is  an  important  element  in 
the  prognosis.  The  symptoms  may  be  due  to  the  activity  of 
some  new  factor  out  with  the  heart  itseh,  to  a  progressive 
lesion  of  the  valve,  or  to  the  development  of  some  patho 
logical  condition  of  the  cardiac  muscle. 

Extrinsic  factors  are  numerous.  Physical  exertion,  whether 
short  and  severe,  or  moderate  and  prolonged;  bronchitis, 
pneumonia,  etc.,  throwing  extra  strain  upon  the  right  heart; 
a  gastro-intestinal  upset  or  an  alcoholic  debauch;  an  attack 
of  influenza;  anaemia  or  debilitj-  pregnancy  and  parturition; 
a  mental  shock  or  business  worries ;  so  often  precede  the  onset 
of  cardiac  symptoms  that  their  relationship  to  it  can  hardly 
be  in  doubt.     Progressive  lesions  occur  both  in  acute  endo- 


368  DISEASES  OF  THE  HEART 

carditis  and  in  the  degenerative  chronic  forms,  and  though 
usually  gradual  in  their  onset,  may  be  sudden,  if,  for  example, 
a  cusp  ruptures  suddenly.  Eatty  overgrowth  and  degenera- 
tion and  fibrosis  of  the  myocardium,  are  usually  of  insidious 
origin,  but  a  sudden  blocking  of  a  coronary  branch  may  produce 
symptoms  with  great  rapidity. 

^  The  prognosis  in  the  individual  case  varies  accordingly. 
The  possibility  of  a  future  pregnancy  can  be  prevented;  the 
patient  may  become  teetotal;  the  occupation  majr  be  changed, 
or  excessive  work  and  strain  may  be  avoided;  and  climatic 
change  may  retard  the  recurrence  of  pulmonary  disease. 
The  fatty  overgrowth  may  be  reduced  by  the  cessation  of 
"indulgence,  indolence,  and  intemperance  ";  an  anaemia  may 
be  overcome;  while  but  little  can  be  effected  in  checking  the 
rapid  progress  of  an  acute  endocarditis,  or  the  insidious  pro- 
gression of  the  more  chronic  lesions  which  are  affecting  the 
valves  or  the  coronary  arteries. 

In  other  cases  failure  is  due  to  the  inception  of  a  new  cardiac 
rhythm,  auricular  fibrillation,  heart-block,  paroxysmal  tachy- 
cardia, etc.  The  prognosis  in  this  event  is  always  serious 
unless  the  progress  of  the  case  reveals  the  individual  tendency 
towards  convalescence.  It  may,  however,  be  borne  in  mind 
that  none  of  the  abnormal  rhythms  are  necessarily  incompatible 
with  life,  which  may  be  prolonged  over  a  period  of  years. 
*^  8.  Ttie,  Age,  of  the  Patient. — The  age  of  the  patient  musFlje 
taken  into  account.  There  is  a  maxim  in  my  insurance  office 
that  in  youth  the  family  history,  in  adult  life  the  habits,  and 
in  later  years  the  circumstances,  of  proposers  should  be  closely 
scrutinized;  and  the  maxim,  on  the  whole,  holds  good  with 
regard  to  the  prognosis  in  cardiac  disease.  A  family  tendency 
to  rheumatism;  habits  of  excess,  whether  at  work  or  at  play, 
in  food  or  in  drink;  the  anxieties  of  straitened  circumstances ; 
are  all  necessarily  untoward  elements  in  the  case. 

Muscular  hypertrophy  in  early  life  is  easily  produced,  and 
is  generally  ample;  but  the  probability  of  recurrence  of  a  rheu- 
matic infection  is  considerable  in  the  teens  and  in  the  twenties, 
when  it  is  most  often  accompanied  by  a  fresh  endocarditis.  If 
growth  is  incomplete,  its  extra  strain  is  badly  borne,  and  a 
considerable  lesion  is  generally  followed  by  a  stunted  develop- 
ment   and   a  poor   physique.      In   elderly  persons   muscular^ 


PROGNOSIS  OF  CHRONIC  VALVULAR  DISEASE     369 

hypertrophy  is  often  limited  in  the  case  of  the  heart,  as  it  is 
in  the  systemic  muscles,  and  compensation  may  be  effected 
with  difficulty.  Other  viscera,  too,  are  apt  to  be  damaged, 
and  the  lungs,  the  kidneys,  or  the  arteries,  are  frequently 
abnormal.  The  nutritional  demand,  on  the  other  hand,  is 
lessened.  The  condition  of  the  ribs  is  probably  important.  In" 
childhood,  when  they  are  soft  and  yielding,  the  contour  of  an 
enlarged  heart  may  be  mapped  out  on  the  front  of  the  chest ; 
but  in  elderly  people,  protrusion  is  unusual,  and  the  heart  can 
only  enlarge  at  the  expense  of  the  other  organs  within  the 
thorax.  On  the  whole,  early  adult  life  is  the  least  unsatis- 
factory age,  for  the  strain  of  growth  is  past,  and  the  prob- 
abihty  of  a  fresh  infection  is  less,  while  muscular  hj^pertrophy 
is  likely  to  be  ample,  and  the  other  viscera  are  probably  sound. 
The  unsatisfactory  feature  is  the  activity  of  manhood,  and  a 
physiological  mean  must  be  carefully  enjoined. 

9.  The  Sex  of  the  Patient. — The  influence  of  sex  is  not  very 
considerable;  for  while  women  as  a  rule  escape  extremes  of 
heat  and  cold,  and  the  strenuous  physical  exertions  to  which 
men  are  so  often  exposed  by  reason  of  their  special  occupation, 
the  gain  is  counterbalanced  by  their  maternal  functions. 
Pregnancy,  in  my  experience,  is  always  a  dangerous  experi- 
ment in  women  who  are  the  subjects  of  chronic  valvular 
disease.  Failure  often  occurs  in  the  later  months  or  following 
child-birth  during  lactation,  though,  curiously  enough,  it  does 
not  seem  to  be  particularly  related  to  the  accouchement. 
It  may  be  due  to  general  debihty  or  to  a  fresh  endocarditis, 
or  to  a  renal  complication.  The  latter  two  are  the  most  fre- 
quent causes.  The  cases  already  recorded  instance  the 
connection. _ 

10.  The  Social  Circumstances  and  Habits  of  the  Patient. — 
The  habits  and  social  circumstances  of  the  patient  are  im- 
portant. Arduous  employments  are,  of  course,  always  in- 
jurious to  patients  whose  cardiac  reserve  is  hmited  by  valvular 
disease;  but  they  may  be  the  only  means  of  obtaining  a  liveh- 
hood ;  and  those  in  receipt  of  a  weekly  wage  are  rarely  able 
to  secure  the  just  medium  of  mental  and  physical  work  that 
is  so  desirable.  The  prognosis  in  hospital  cases  is  in  con- 
sequence less  favourable  than  in  private  patients. 

24 


CHAPTER  XXVI 
THE  TREATMENT  OF  CHRONIC  CARDIAC  FAILURE 

The  general  indications  for  treatment  in  cases  where  com- 
pensation has  broken  down  are  comparatively  clear.  The  heart 
must  he  relieved  of  all  unnecessary  work,  and  its  nutrition  must 
be  improved.  Symptoms  ivhich  by  their  presence  throw  a  strain 
upon  the  heart  must  be  relieved.  Cardiac  stimulation  may  be 
required. 

1.  Considerable  rehef  is  almost  always  experienced  after  the 
cardiac  work  has  been  reduced  to  a  minimum  by  confining  the 
patient  wholly  to  bed,  under  the  charge  of  an  efficient  nurse 
(Fig.  185).  In  no  other  way  can  the  unnecessary  work  be  so 
thoroughly  removed,  for  the  rate  of  the  pulse  is  always  in- 
creased when  the  patient  is  even  sitting  up,  and  if  5  beats  per 
minute  are  saved,  it  means  7,200  beats  in  the  twenty-four 
hours.  The  patient's  comfort,  however,  must  be  consulted, 
for  discomfort  means  restlessness,  and  restlessness  entails  work, 
and  support  by  means  of  pillows  or  a  bedchair  is  required  in 
cases  where  orthopnoea  exists.  In  the  lesser  degrees  of  failure, 
of  course,  such  restrictions  are  unnecessary,  and  the  patient 
may  be  able  to  sit  quietly  at  home  or  to  take  a  hmited  amount 
of  exercise,  but  the  desired  result  is  attained  most  quickly  by 
absolute  confinement  to  bed ;  and  it  is  always  easy  to  diminish 
restrictions,  while  it  is  often  difficult  to  increase  them.  The 
rationale  is  simple:  the  expenditure  must  be  curtailed  until 
the  overdraft  is  paid  off,  and  when  this  is  accomphshed,  must 
be  rearranged  on  such  a  scale  that  the  income  is  not  exceeded. 

The  rest,  too,  must  be  mental  as  well  as  physical,  for  mental 
worry  and  strain  entail  extra  work  to  the  heart,  as  the  blood- 
pressure  is  thereby  raised  and  the  pulse-rate  is  often  increased. 

The  return  to  ordinary  habits,  when  convalescence  is  estab- 

370 


TREATMENT   OF  CHRONIC  CARDIAC  FAILURE     371 

lished,  must  always  be  gradual  and  should  be  closely  super- 
vised, so  that  any  injurious  results  may  be  at  once  recognized. 
It  is  often  helpful  to  have  patients  massaged  mildly  when  they 
are  still  confined  to  bed  and  its  effects  can  be  readily  estimated; 
and  the  general  improvement  in  nutrition  which  it  produces 
as  a  rule  shortens  the  subsequent  con- 
valescence. 

It  is  impossible  to  lay  down  absolute 
rules  as  to  the  period  for  which  patients 
should  be  confined  to  bed,  but  it  is 
never  wise  to  allow  them  out  of  bed 
until  all  the  symptoms  are  in  abeyance, 
and  the  pulse-rate  is  again  normal,  and 
the  confinement  should  even  then  be 
continued  for  one  or  two  or  even  three 
weeks  longer.  In  elderly  people,  how- 
ever, severe  restrictions  are  sometimes 
badly  borne,  confinement  to  bed  pro- 
ducing loss  of  appetite,  sleeplessness, 
mental  depression,  etc.,  and  it  is  some- 
times wise  in  these  cases  to  allow  the 
amount  of  exertion  to  be  determined 
by  the  patient  himself  rather  than  by 
his  medical  attendant. 
ji  2.  A  priori  a  weak  heart  requires 
more  nourishment  than  a  healthy  one, 
so  that  in  cardiac  failure  every  effort 
should  be  made  to  insure  an  adequate 
supply ;  but  the  digestive  disturbances 
which  so  often  co- exist  may  render  the 

task  difficult.  In  serious  failure  the  symptoms  are  frequently 
intensified  by  abdominal  distension,  vomiting,  and  flatulence; 
diarrhoea  is  uncommon.  The  dietary,  in  consequence,  must  be 
of  a  kind  that  throws  little  work  upon  the  digestive  organs .  The 
carbohydrates  and  the  vegetables  are  generally  contra-indicated 
on  this  account,  for  both  are  liable  to  produce  flatulence,  and 
while  the  latter  notoriously  entail  extra  work,  the  absence  of 
oral  digestion  in  serious  cases  is  Ukely  to  disturb  the  proper 
digestion  of  the  former.     Milk  is  usually  well  borne  in  these 


Fig.  185. — Arterio-Sclebo- 
sis;  Auricular  Fibrilla- 
tion; Cardiac  Faxlube. 

Dec.    4:    (Edema    universal 

and  considerable. 
Dec.    10:    Qiidema  minimal. 

-  -  -  urinary    output    in 

ounces;   — ==  pulse-rate. 
Treatment:  Rest  in  bed  and 

a  simple  alkaline  mixture. 


372  DISEASES  OF  THE  HEART 

cases,  and  should  be  given  in  small  quantities  and  frequently 
(every  two  to  three  or  four  hours  during  the  day,  and  every 
four  or  five  hours  at  night).  It  may  be  predigested  or  diluted, 
or  flavoured  with  weak  tea,  coffee,  rum,  etc.;  3  or  4  pints  may 
be  given  in  the  twenty-four  hours.  Benger's  or  Mellin's  food 
can  sometimes  be  added  with  benefit. 

If  the  tongue  is  clean  and  the  stools  normal,  solid  food  may 
be  given,  small,  lean,  fine-fibred  fishes,  such  as  whiting,  had- 
dock, and  sole,  the  breast  of  young  birds,  and  eggs  lightly 
boiled  or  poached,  being  the  most  suitable.  Carbohydrates 
should  be  given  in  minimal  amount  and  in  dry  form — toast, 
rusks,  biscuits,  etc. — so  as  to  insure  thorough  mastication. 
The  amount  of  solid  food  at  first  should  be  small,  so  as  to  avoid 
undue  distension  of  the  stomach.  As  the  quantity  of  sohd 
food  is  increased,  the  intake  of  milk  may  be  correspondingly 
diminished. 

The  cooking  of  the  food  must  be  of  the  simplest  kind,  but 
as  much  variety  as  is  possible  should  be  secured,  so  as  to  in- 
crease the  psychic  appetite;  and  it  may  be  remembered  that 
a  fried  fish,  free  of  its  batter  and  oil,  is  just  as  digestible  as,  and 
infinitely  more  appetizing  than,  one  which  has  been  plainly 
boiled.  The  clear  and  the  thick  soups  are  generally  inad- 
visable, but  stewed  fruit  (apples,  pears)  may  be  useful  as  a 
medium  for  the  consumption  of  cream. 

The  intake  of  fluids  requires  regulation.  In  many  cases 
dropsy  is  present,  and  it  seems  desirable  to  limit  the  intake  of 
water;  but  in  many  patients  renal  complications  co-exist,  and 
the  blood-pressure  is  high,  and  the  intoxication  is  best  remedied 
by  the  administration  of  fluid  in  sufficient  amount.  The 
estimation  of  the  blood-pressure  is  all-important  from  the 
point  of  view  of  treatment ;  for  if  it  is  high,  free  elimination 
must  be  secured  before  any  good  result  will  be  obtained.  In 
young  people,  however,  the  kidneys  are  generally  normal,  and 
the  intake  of  fluid  may  be  restricted  with  benefit.  The 
amount  taken  at  meals  should  always  be  small  (less  than 
10  ounces),  so  as  not  to  interfere  with  digestion. 

A  similar  distinction  must  be  made  with  regard  to  the  con- 
sumption of  table  salt.  In  acute  nephritis  and  in  many  cases 
of  chronic  nephritis  the  excretion  of  salt  is  deficient,  and  it 


TREATMENT  OF  CHRONIC  CARDIAC  FAILURE     373 

accumulates  in  the  tissues,  and  to  keep  the  fluids  of  the  body 
isotonic  attracts  fluid  to  the  parts.  The  resultant  dropsy  can 
be,  in  part  at  any  rate,  relieved  by  the  withdrawal  of  salt 
from  the  diet.  In  cardiac  cases  with  high  blood-pressure  salt 
retention  frequently  occurs,  and  its  intake  should,  in  conse- 
quence, be  restricted.  Less  than  a  gramme  of  salt  daily  is 
required  by  a  healthy  individual,  who,  however,  habitually 
exceeds  this  amount,  sometimes  to  a  very  notable  degree. 
Salt  is  present  in  bread  and  in  almost  all  cooked  dishes,  if 
one  excludes  sweets  from  the  hst.  Its  use  in  bread  and  in 
cooking  should  be  interdicted,  and  the  amount  used  at  table 
carefully  restricted  to  less  than  the  normal  requirement  of  a 
gramme. 

In  elderly  persons  a  sudden  and  complete  change  of  diet  is 
often  badly  borne,  being  apt  to  produce  anorexia  or  indigestion 
of  varying  type  and  degree.  The  patient's  habits  in  this 
respect  should  be  considered,  and  a  detailed  list  of  the  articles 
of  food  which  are  habitually  consumed  will  generally  be  found 
to  contain  some  elements  which  are  relatively  innocuous.  The 
use  of  tea  and  alcohol,  for  example,  should  often  be  continued, 
though  the  amount  or  the  quahty  may  require  to  be  altered. 

Balfour  recommended  the  following  "  dry  "  dietary  in  cases 
of  senile  heart  when  there  is  anasarca : 

Breakfast. — A  single  slice  of  dry  toast  with  no  butter,  and 
4  ounces  of  tea  infused  for  not  more  than  four  minutes,  with 
cream  and  sugar. 

Dinner. — Not  more  than  the  lean  of  two  chops  or  their 
equivalent  in  fish  or  chicken;  no  vegetables ;  as  much  dry  toast 
as  may  be  desired,  and  \  ounce  of  spirits  in  3  ounces  of  water. 

Supper. — As  much  dry  toast  as  is  desired,  and  ^  ounce  of 
spirits  in  3  ounces  of  water. 

He  did  not  consider  that  it  was  advisable  that  a  patient  in 
this  condition  should  drink  much,  even  between  meals,  and 
only  allowed  3  to  4  ounces  of  hot  water,  sipped  slowly,  about 
an  hour  before  each  meal.  A  dietary  so  restricted  is,  however, 
rarely  well  borne  for  any  length  of  time  in  chronic  heart 
disease,  the  restriction  of  fluids  in  particular  leading  to  much 
discomfort;  but  the  consumption  of  2  pints  of  fluid  in  the 
twenty-four  hours  is  generally  tolerated. 


374  DISEASES  OF  THE  HEART 

The  following  diets  are  in  use  in  my  wards,  and  are  generally 
useful.  In  private  practice  they  have  usually  to  be  modified, 
but  the  general  idea  can  be  maintained.  The  chief  meal 
should  be  taken  in  the  middle  of  the  day.  The  patient  should 
rest  quietly  for  at  least  half  an  hour  after  the  larger  meals,  and 
for  the  same  period  before  them,  and  efficient  mastication  must 
be  insisted  upon.  Every  effort  should  be  made  to  insure  a 
sufficient  variety  in  the  foodstuffs,  so  as  to  encourage  appetite, 

"  Cardiac  "  Diet. 

5  a.m. :  Milk,  8  ounces;  bread-and-butter,  2  ounces. 

8  a.m.:  Tea,  8  ounces;  bread-and-butter,  6  ounces;  fish,  4  ounces,  or  a 
lightly  boiled  or  poached  egg. 

11  a.m. :  Milk,  8  ounces,  or  milk  and  Benger's  food,  or  a  switched  egg. 

I  p.m.:  Chicken,  boiled  or  roast  mutton,  4  ounces;  bread,  4  ounces; 
milk  pudding,  6  ounces. 

5  p.m. :  Milk  pudding  or  tea,  8  ounces;  bread-and-butter,  6  ounces. 

7  p.m. :  Milk,  8  ounces;  bread-and-butter,  4  ounces. 

The  bread  is  stale  and  toasted.  The  diet  is  free  from  salt, 
which  is  added  at  the  table  if  ordered.  The  total  fluid  may  be 
restricted  to  30  ounces.  Milk  pudding  includes  cornflour, 
ground  rice,  semofina,  tapioca,  sago,  arrowroot,  custard.  Milk 
may  be  made  more  digestible  by  being  citrated,  "soured,"  or 
peptonized,  and  more  palatable  by  the  addition  of  weak, 
freshly  infused  China  tea  or  coffee  as  flavouring  agents,  or  may 
be  given  in  the  form  of  curds  or  junket. 

"  Light"  Diet. 
5  a.m. :  Milk,  10  ounces. 

8  a.m.:  Milk,  or  milk  and  weak  tea,  10  ounces;  bread-and-butter,  2  to  8 
ounces;  white  fish,  4  ounces,  or  an  egg  lightly  boiled  or  poached. 

II  a.m.:  Milk  or  Benger's  food,  10  ounces. 

1  p.m. :  Chicken  or  white  soup,  10  ounces;  chicken  or  white  fish,  4  ounces; 
potatoes,  2  ounces ;  vegetables,  1  ounce  (cauliflower,  cabbage,  sprouts);  bread, 
1  ounce ;  milk  pudding,  10  ounces. 

5  p.m.:  Milk,  or  weak  tea  and  milk,  10  ounces;  bread-and-butter,  2  to  8 
ounces ;  white  fish,  4  ounces,  or  an  egg. 

8  p.m. :  Milk,  8  ounces.     Cream,  10  ounces  per  diem. 

This  diet  is  salted. 

3.  The  Treatment  of  Symptoms. — The  relief  of  particular 
symptoms  is  often  a  necessary  antecedent  to  any  real  improve- 
ment, for   dropsy,  pain   or   sleeplessness   may  of   themselves 


TREATMENT   OF  CHRONIC  CARDIAC  FAILURE     375 

prevent  that  rest  which  is  so  essential.  In  the  shghter  degrees 
of  dropsy  it  may  be  sufficient  to  keep  the  bowels  loose,  but  in 
the  graver  forms  the  fluid  should  be  removed  without  delay, 
accumulations  in  the  serous  sacs  being  removed  by  a  trocar 
and  canula,  and  subcutaneous  oedema  by  multiple  puncture, 
which  is  generally  preferable  to  the  use  of  Southey's  tubes^ 
The  punctures  should  be  numerous,  but  separated  from  each 
other  by  an  inch;  two  or  three  rows  may  be  made  on  each 
side  of  the  legs  below  the  knees.  The  punctures  should  not 
be  deep,  merely  through  the  skin,  the  needle  being  "  guarded  " 
by  the  finger  and  thumb  finch  from  the  point.  With  a  sharp, 
broad  surgical  needle  the  stabs  may  be  made  with  great 
rapidity  and  occasion  little  pain.     Asepsis  must,  of  course,  be 

maintained.  , 

The  dyspnoea,  which  so  frequently  aggravates  a  patient's 
sufferings,  is  often  extremely  difficult  to  treat.  It  may  be 
due  to  bronchitis,  to  even  small  amounts  of  fluid  in  the 
pleural  sacs,  to  oedema  of  the  lungs,  or  to  toxic  causes;  but, 
however  caused,  may  interfere  gravely  with  sleep  and  rest. 
Much  can  be  done  by  suitable  bed-rests,  etc.,  to  make  the 
patient  comfortable  sitting  up  in  bed,  but  in  some  cases  a 
chair  affords  more  ease,  though  in  the  latter  case  any  oedema 
in  the  legs  is  generally  increased.  Oxygen  is  sometimes  help- 
ful. If  there  is  fluid  in  the  chest,  it  should  be  removed,  even 
though  but  half  a  pint  can  be  taken  away ;  while  bronchitis  may 
be  helped  by  the  usual  means.  (Edema  of  the  lungs  can  only 
be  remedied  b}'  improvement  of  the  cardiac  condition;  but  in 
the  toxic  cases  much  relief  may  be  obtained  by  the  use  of 
mercury  and  morphia,  the  former  being  given  as  blue  pill  or 
calomel  in  sufficient  amount  to  secure  two  or  three  loose  stools 
in  the  day,  and  the  latter  hypodermically  and  combined  with 
atropine.-  The  dose  of  morphia  at  first  should  be  small  (gr.  |to  Jr), 
but  it  may  be  increased  if  well  borne.  It  rarely  occasions  trouble, 
though  care  must  be  exercised  if  there  is  much  secretion  in 
the  bronchi,  or  if  the  urine  is  scanty  and  highly  albuminous. 
A  similar  hne  of  treatment  is  often  useful  in  sleepless  patients. 
Insomnia  is  frequently  accompanied  by  dyspnoea  and  by  great 
restlessness,  and  is  but  rarely  benefited  by  the  usual  h3-pnotics. 
A  dose  of  bromide  in  hot  whisky  may  be  sufficient  in  the  milder 


376  DISEASES  OF  THE  HEART 

cases,  and  may  be  backed  up  by  chloral.  Paraldehyde  also  is 
useful  at  times.  In  chronic  cases,  however,  morphia  is  in- 
valuable, and  improvement  is  often  rapid  after  two  or  three 
good  nights'  sleep  have  been  obtained.  In  high-pressure  cases  , 
W.  RusseU  finds  vaso-dilator  drugs  useful.  Similar  treatment 
may  be  required  for  cough,  but  the  cough  of  irritation  must 
be  distinguished  from  that  associated  with  profuse  secretion; 
and  while  morphia  is  indicated  in  the  first  case,  it  is,  of  course, 
prejudicial  in  the  second.  Haemoptj^sis  rarely  occasions 
anxiety,  and  generally  ceases  without  treatment,  though  in 
infarct  the  spit  may  continue  to  be  blood-stained  for  a  week 
or  more. 

The  milder  degrees  of  cardiac  discomfort  are  generally  re- 
Heved  by  local  appHcations — hot  fomentations,  blisters,  anti- 
phlogistin,  an  ice  poultice,  etc. — but  if  severe,  require  opium 
in  some  form.  The  pain  of  hepatic  congestion  is  best  treated 
by  dry-cupping  followed  by  hot  poultices,  or  by  leeching,  the 
bowels  being  kept  active  by  mercurials. 

Gastro  -  intestinal  symptoms  sometimes  entail  anxiety, 
especially  if  vomiting  is  repeated  and  severe,  and  interferes 
with  nutrition.  Here,  again,  mercurials  are  most  hkely  to  be 
of  use,'  and  it  often  lessens  as  soon  as  the  bowels  have  been 
freely  moved;  a  mustard  poultice  over  the  epigastrium  some- 
times helps.  Whey,  albumin  water,  and  weak  tea  are  most 
likely  to  be  retained.  The  usual  gastric  sedatives  are  of  httle 
value.  In  severe  repeated  vomiting  water  is  often  weU  borne 
and  may  be  retained,  at  any  rate  in  part,  even  when  all  food 
is  rejected.  Even  if  it  is  returned,  it  flushes  out  the  stomach 
and  frequently  makes  the  patient  less  uncomfortable. 

4.  The  action  of  digitalis,  as  shown  in  animals,  is  somewhat 
comphcated,  as,  besides  its  local  irritant  action,  it  affects  the 
central  nervous  system,  the  heart,  and  the  arteries.  It  stimu- 
lates the  medullary  centres,  slowing  the  rate  of  the  heart  and 
lessening  its  tone  and  constricting  the  arteries.  It  strengthens 
and  prolongs  ventricular  systole  by  its  direct  action  upon 
the  heart,  and  increases  its  muscular  tone,  so  that  relaxation 
is  less  complete;  and  it  exalts  its  irritabihty.  It  produces 
constriction  of  the  arteries  directly  as  weU  as  through  the 
nervous  system.     The  ultimate  result,  however,  varies,  as  the 


TREATMENT  OF  CHRONIC  CARDIAC  FAILURE     377 

nervous  and  cardiac  mechanisms  are  in  some  ways  opposed. 
With  small  doses  the  cardiac  contractions  become  less  frequent 
but  more  complete,  so  that  the  ventricular  output  is  increased, 
and  the  arterial  pressure  is  raised.  With  larger  doses  the 
inhibitory  action  is  augmented,  the  contractions  become  less 
frequent  and  perhaps  irregular,  and,  though  diastohc  relaxa- 
tion becomes  more  ample,  the  ventricular  output  lessens. 
With  increasing  doses  the  excitabihty  is  so  exalted  that  the 
pulse-rate  becomes  very  frequent,  and  the  auricles  may  pass 
into  fibrillation,  while  the  ventricular  action  becomes  irregular 
and  the  output  is  still  further  diminished.  The  irregularity 
may  be  due  to  several  causes.  The  whole  heart  may  be  con- 
cerned if  it  is  produced  by  medullary  inhibition,  or  the  ven- 
tricles alone  if  heart-block  or  auricular  fibrillation  ensue. 

The  crisp  results  obtained  in  experiment  on  normal  hearts 
do  not,  however,  convey  as  precise  indications  for  the  use  of 
digitahs  in  actual  practice  as  might  be  anticipated,  as  the 
hearts  concerned  are  never  normal,  and  in  cardiac  failure  the 
whole  metabohsm  of  the  patient  is  often  out  of  gear.  The 
uses  of  digitahs  have  to  be  determined  by  actual  experience 
in  sick  people. 

Withering 's  remarks  on  the  "  constitution  of  patients  "  in 
his  "Account  of  the  Foxglove"  are  extremely  interesting. 
"  Digitalis,"  he  says,  "  seldom  succeeds  in  men  of  great  natural 
strength,  of  tense  fibre,  of  warm  skin,  of  florid  complexion,  or 
in  those  with  a  tight  and  cordy  pulse.  If  the  belly  in  ascites 
be  tense,  hard,  and  circumscribed,  or  the  limbs  in  anasarca 
sohd  and  resisting,  we  have  but  little  to  hope.  On  the  contrary, 
if  the  pulse  be  feeble  and  intermitting,  the  countenance  pale, 
the  lips  livid,  the  skin  cold,  the  swollen  belly  soft  and  fluctuat- 
ing, or  the  anasarcous  limbs  readily  pitting  under  the  pressure 
of  the  finger,  we  may  expect  the  diuretic  effects  to  follow  in 
a  kindly  manner."  Translated  into  current  phraseology, 
Withering's  remarks  mean  that  digitahs  is  not  hkely  to  prove 
helpful  in  cases  of  dropsy  with  high  arterial  pressure,  and  that 
it  is  hkely  to  be  of  value  if  auricular  fibrillation  has  ensued.  ^.^^-^ 

The  first  point  which  should  be  determined  in  every  case-of 
cardiac  failure  is  the  height  of  the  blood-pressure.  A  sphyg- 
momanometer is  not  required — the  finger  alone    can  decide 


378  DISEASES  OF  THE  HEART 

the  point — for  if  the  blood-pressure  is  high,  ehminative  treat- 
ment is  required,  and  digitals  will  fail  unless  it  is  accompanied 
or  preceded  by  treatment  of  this  kind.  A  hundred  j-ears  after 
Withering  wrote,  Wilham  Murray  discussed  the  point  as 
follows :  "  The  administration  of  (mercury)  in  cardiac  dropsy 
...  is  as  old  as  the  hills,  and  we  old-fashioned  physicians  know 
well  enough  that  thirty  or  forty  years  ago  no  one  thought  of 
treating  those  conditions  except  by  a  mercurial  pill,  followed 
by  a  saline  or  jalap  purgative,  and  a  diuretic  mixture  con- 
taining digitalis."  The  actual  height  of  the  blood-pressure 
is  immaterial.  Digitahs  frequently  acts  well  in  cases  where 
it  is  greatly  above  normal,  if  it  is  combined  with  treatment  of 
the  kind  suggested  by  Dr.  Murray;  and,  if  it  is  permissible, 
the  administration  of  digitalis  may  be  delayed  with  advantage 
for  two  or  three  days. 

There  is,  of  course,  the  risk  that  digitahs  in  these  cases  may 
produce  such  an  elevation  of  the  blood-pressure  that  a  cerebral 
vessel  ruptures .  I  am  not  aware  of  such  an  accident  in  my  own 
experience,  and  I  am  at  one  with  James  Mackenzie  in  his 
statement  that  medicinal  doses  comparatively  rarely  affect 
the  blood-pressure  to  any  appreciable  degree.  It  is  always 
wise  to  administer  digitahs  in  a  simple  diuretic  mixture — for 
example,  in  combination  with  citrate  of  potassium  and  Hquor 
ammoniae  acetatis,  or  with  iodide  of  potassium;  or  the  weU- 
known  Guy's  piU  may  be  utihzed. 

The  question  has  aheadj"  been  discussed  in  detail  (p.  84) 
in  connection  with  arterio-sclerosis,  which,  I  would  again 
remind  the  reader,  is  very  often  associated  with  valvular 
disease  of  the  heart.  Of  other  drugs  in  these  cases  caffeine 
citrate  and  diuretin  are  probablj^  the  most  useful.  G.  A. 
Gibson  recommended  the  combination  of  potassium  citrate, 
caffeine  citrate,  and  infusion  of  digitahs,  which  I  have  used 
with  success. 

The  majority'  of  writers  state  that  digitahs  is  often  useless 
in  senile  heart  disease,  and  consider  that  this  is  due  to  fibroid 
or  other  disease  of  the  cardiac  muscle.  The  fact  is,  of  course, 
weU  known;  but  the  failure  of  digitalis  is  more  often  due  to 
associated  arterio-sclerosis  and  imperfect  elimination  than  to 
actual  disease  of  the  m^^ocardium. 


TREATMENT   OF  CHRONIC  CARDIAC  FAILURE     379 

The  occurrence  of  a  weak,  irregular  puLse  in  dropsy  was  stated 
by  Withering  to  be  an  indication  for  the  use  of  digitahs.  Sir 
WiUiam  Broaclbent  gave  a  more  detailed  description,  stating 
that  a  frequent  weak,  irregular  pulse,  accompanied  by  oedema 
and  a  scanty,  concentrated,  turbid  urine,  were  the  special 
indications;  and  James  Mackenzie,  anatyzing  his  results  from 
the  standpoint  of  the  varying  rhj'thms  that  may  be  met  with 
in  cardiac  failure,  states  that  it  is  most  useful  in  auricular 
fibrillation  the  pulse-rate  slowdng  concurrently  with  improve- 
ment, though  the  irregularity  persists,  ~^ 

The  slowing  of  the  pulse-rate  in  these  cases  seems  to  be  due 
to  direct  action  of  the  drug  upon  the  heart,  and  not  to  stimu- 
lation of  the  inhibitory  mechanism,  as  the  rate  is  not  affected 
by  atropine  (Cushny),  and  it  is  most  probably  due  to  depres- 
sion of  conductivity,  though  it  might  result  from  a  lessening 
of  excitability.  In  cases  with  a  normal  rhj^thm,  where  the 
pulse-rate  is  slowed,  the  atropine  results  are  variable,  so  that 
in  some  cases  the  slowing  is  due  to  direct  action  upon  the  heart, 
in  others  to  inhibition.  In  cases  with  a  normal  rhythm,  the 
beneficial  results  of  digitalis  are  rarely  accompanied  by  such 
striking  effects  upon  the  pulse-rate  as  are  seen  in  auricular 
fibrillation.  The  improvement  in  the  tone  of  the  heart  which 
the  drug  produces  is  probabl}-  the  chief  factor  in  the  bene- 
ficial results,  and  a  dilated  heart  often  shrinks  rapidly  under 
its  administration.  The  frequency  of  the  pulse  of  fever, 
exophthalmic  goitre,  acute  endocarditis,  etc.,  is  seldom  in- 
fluenced to  any  notable  degree,  though  the  other  good  results 
may  be  well  marked.  Even  as  I  write,  its  value  in  fever  has 
been  well  exemphfied.  A  man  aged  thirty-nine  was  admitted 
into  my  wards  on  the  fifth  day  of  a  pneumonia.  He  was 
shghtly  jaundiced,  and  very  prostrate,  the  puLse  being  soft 
and  quick,  and  the  second  sound  at  the  puhnonar}'  area  less 
emphatic  than  the  first.  Forty-eight  hours  later,  coincidently 
with  the  administration  of  digitalis,  the  pulse  was  stronger 
and  less  quick,  though  the  rate  had  not  decreased,  and  it  was 
still  running  about  120;  the  second  sound  had  become  em- 
phatic. During  the  crisis  on  the  eighth  day  the  heart  for  a 
few  hours  showed  signs  of  failure,  but  it  quickly  recovered, 
and  convalescence  was  good. 


380  DISEASES  OF  THE  HEART 

It  is  necessary  to  administer  considerable  doses,  and  to 
push  the  drug  until  either  the  desired  result  is  obtained  or 
symptoms  of  intolerance  appear.  The  old  rule  that  nausea  or 
vomiting  increased  frequency  of  the  pulse,  and  diminution  in 
the  output  of  urine,  indicate  cessation  of  the  drug,  is  a  useful 
guide,  and  dangerous  symptoms  will  never  appear  if  it  is 
observed.  The  administration  should  also  be  stopped  if  the 
pulse-rate  falls  to  50. 

The  dangers  of  digitalis  are  in  all  probability  exaggerated. 
In  myocardial  disease  sudden  death  is  not  uncommon,  but 
its  occurrence  when  the  patient  is  taking  digitalis  is  not 
necessarily  the  result  of  the  drugging.  Balfour  quoted  a  case 
in  which  death  ensued  after  211  grains  of  the  powdered  leaves 
had  been  taken  within  five  weeks;  but  marked  symptoms  of 
intolerance  had  been  present  for  four  weeks  previous  to  death  I 
I  have  only  seen  one  case  in  which  sudden  death  ensued  during 
its  administration,  and  in  which  the  drug  might  perhaps  be 
blamed  for  the  result.  The  patient,  who  was  not  under  my 
care,  was  suffering  from  symptoms  of  cardiac  weakness, 
which  had  followed  the  excessive  use  of  beer.  There  was 
no  valvular  disease,  but  the  heart  was  very  large.  Under 
full  doses  of  digitalis  the  symptoms  were  relieved,  and  the 
pulse-rate  fell  to  about  50.  There  were  no  symptoms  of 
intolerance  otherwise;  but  he  died  suddenly  one  morning  after 
getting  up  out  of  bed. 

James  Mackenzie  recommends  a  daily  dose  of  1  drachm  of 
the  tincture  divided  into  three  or  four  equal  doses.  Smaller 
amounts,  in  my  experience,  are  generally  sufl&cient— 20  or 
30  minims  in  the  day — and  I  rarely  find  it  necessary  to  ad- 
minister the  larger  dose.  The  effects  are  not  noticeable  for 
three  or  four  days.  In  the  majority  of  patients  a  good  result 
is  obtained  when  the  pulse-rate  reaches  normal,  but  some 
pa^iients  experience  most  benefit  when  it  is  still  lower;  and 
BaKour  stated  that  he  had  successfully  kept  the  pulse  running 
for  days  at  40.  Such  cases  are,  however,  exceptional.  The 
appearance  of  a  coupled  rhythm  is  an  indication  of  approaching 
intolerance. 

When  the  symptoms  have  disappeared  and  the  pulse-rate 
is  within  normal  limits,   the  dose  may  generally  be  discon- 


TREATMENT   OF  CHRONIC  CARDTAC  FAILURE     381 

tinued,  and  general  tonics  substituted.  But  in  some  patients 
digitalis  seems  to  be  necessary  to  their  comfort.  A  woman 
who  was  recently  in  my  wards  suffering  from  mitral  disease 
and  auricular  fibrillation  stated  that  she  had  taken  digitalis 
regularly  for  seven  years.  Improvement  was  rapid  after  her 
admission  to  hospital,  and  the  drug  was  stopped.  But  as 
soon  as  she  went  to  a  convalescent  home  the  symptoms 
recurred,  though  they  were  readily  kept  in  abeyance  by 
regular  minimal  doses.  Fig.  186  shows  the  relation  of  the 
pulse-rate  to  the  dose  in  another  mitral  fibrillation  case. 
There  were  few  symptoms  present  after  the  first  week  of  her 
residence,  but  cessation  of  the  drug  or  diminution  of  the  dose 
was  rapidly  followed  by  an  increase  in  the  pulse-rate  and  the 
discomforts  of  the  patient,  who  spontaneously  requested  the 
continuance  of  the  drug. 

James  Mackenzie  has  shown  that  heart-block  may  be  pro- 
duced by  digitalis  in  the  clinic  as  in  the  laboratory.  He  has 
utilized  the  reaction  to  prove  the  existence  of  those  partial 
forms  of  block  which  are  not  associated  with  an  intermittent 
pulse,  and  finds  that  the  pulse  can  often  be  made  to  intermit 
in  those  cases,  as  the  block  is  exaggerated,  and  occasional 
impulses  fail  to  pass  through  to  the  ventricle.  In  exceptional 
instances,  with  a  normal  cervical  tracing,  heart-block  may 
also  ensue,  apparently  from  the  existence  of  a  latent  weak- 
ness in  conduction.  The  presence  of  partial  heart-block  is 
thus  a  contra-indication  to  the  use  of  digitalis,  as  the  block 
wiU  be  intensified  by  its  administration.  In  the  chronic 
forms  of  full  heart-block,  however,  this  contra-indication  dis- 
appears . 

In  cases  of  paroxysmal  tachycardia  the  pulse-rate  is  usually 
unaffected  by  digitahs  (always,  in  my  experience);  but  Mac- 
kenzie has  found  that  in  auricular  fiutter  the  auricles  passed 
into  fibrillation  during  its  use,  and  that  on  its  cessation  the 
heart  resumed  its  normal  rhythm. 

Extra-systoles  as  a  rule  are  not  a  contra-indication  to  its 
use,  for  although  they  are  by  no  means  uncommon  when  the 
rate  of  the  contractions  lessens,  their  appearance  is  probably 
more  often  due  to  the  prolongation  of  diastole  than  to  in- 
creased  irritability    of    the   heart.     When   stimuli    occur    at 


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TREATMENT  OF  CHRONIC  CARDIAC  FAILURE     383 

frequent  intervals,  diastole  is  too  short  to  allow  ectopic  stimuli 
to  arise,  and  a  coupled  rhythm  rarely,  if  ever,  occurs  with  a 
pulse-rate  of  over  100,  whether  the  auricles  are  in  fibrillation 
or  contracting  in  response  to  sinus  stimuli. 

The  use  of  digitalis  in  cases  of  aortic  reguj?gitation  has  been 
much  discussed.  Theoretically,  prolongation  of  diastole  in 
these  cases  seems  inadvisable,  as  it  will  increase  the  amount 
of  blood  which  regurgitates  into  the  ventricle ;  but,  as  has  been 
already  mentioned,  failure  of  compensation  in  aortic  cases  is 
due  to  dilatation  of  the  heart,  and  is  often  accompanied  by 
mitral  insufficiency.  The  loss  of  tone  which  is  present  is  an 
indication  for  the  drug,  and  practical  experience  has  shown 
that  much  benefit  is  often  derived  from  its  administration. 

Many  preparations  of  digitalis  have  been  advocated,  but 
the  standardized  tincture,  the  fresh  infusion,  the  NativeUe 
granules,  and  Guy's  (Baillie's)  pill,  are  generally  found  to  be 
efficacious.  It  is  said  that  the  infusion  is  particularly  valu- 
able in  cardiac  dropsy,  and  the  tincture  in  fibrillation,  while  the 
pill  is  indicated  in  cases  with  defective  elimination.  Trous- 
seau's wine  is  a  preparation  which  is  often  well  borne  by 
irritable  stomachs.  Digitalin  may  be  injected  subcutaneously, 
a  procedure  which  is  sometimes  useful  if  sickness  prevents 
oral  administration. 

Gtjy's  OB  Baillie's  Pill, 

'^    Pulv.  digital,  fol.  | 

Pulv,  scillse  J- . .         . .         . .  . .     aa  gr.  i. 

Pil.  hydrarg.        J 

M.  et  ft.  pil. 

ViN  Teotjsseaxt. 

White  wine       , .  . .  . .  . .  750  grammes. 

Squill  bulbs       . .  . .  . .  . .  5         ,, 

Juniper  berries  . ,  . .  , .  50        ,, 

Foxglove  leaves  . .  . .  . .  10        ,, 

Macerate  for  four  days;  then  add  potass,  acet.,  15  grammes,  and  filter. 
Dose:  One  teaspoonful. 

Of  the  other  cardiac  tonics,  strophanthus  and  squill  have  the 
best  reputation,  but  they  rarely  succeed  when  digitahs  has 
failed.  Strophanthus  is  said  to  have  little  action  upon  the 
arterioles,  and  thus  to  be  indicated  in  high  blood-pressure 
cases ;  but  it  is  alleged  to  be  an  irritant  to  the  kidneys,  and  so 


384  DISEASES  OF  THE  HEART 

contra-indicated  when  they  are  abnormal.  Caffeine,  theo- 
bromine (diuretin,  theobromose),  convallaria,  are  also  useful 
in  the  milder  forms  of  failure,  when  a  temporary  change 
of  drug  seems  advisable. 

The  "  diffusible  stimulants  " — ammonia  and  alcohol — ^are  fre- 
quently of  use.  Sal  volatile  is  one  of  the  best  immediate 
stimulants  in  cases  of  faintness,  though  its  continued  use  is 
rarely  of  much  value.  The  general  opinion  of  the  value  of 
alcohol  has  been  corroborated  by  my  own  experience,  notwith- 
standing the  variable  opinions  which  have  been  expressed 
upon  the  subject.  It  may  be  of  more  use  on  account  of  its 
vaso-dilator  than  from  its  stimulant  action.  Hot  fomenta- 
tions applied  over  the  heart  have  an  instantaneous  action. 
"^  The  general  nutrition  of  the  ^patient  must  never  be  for- 
gotten, as  symptoms  of  cardiac  failure  sometimes  ensue  on 
account  of  a  general  failure  in  strength,  and  often  accompany 
anaemia,  however  produced.  Arsenic,  strychnine,  iron,  and 
quinine,  are  frequently  of  value,  in  particular  after  the  acute 
symptoms  of  failure  have  abated  and  convalescence  has 
commenced. 

^  REFERENCES. 

A.  R.  CusHNY  AND  OTHERS:  The  Action  of  Digitalis  in  Therapeutics,    Heart, 

1912-13,  vol.  iv.,  p.  33. 
James  Mackenzie:  Digitalis.    Heart,  1910-11,  vol.  ii.,  p.  273. 
William  Mukray  :  Rough  Notes  on  Remedies,  London,  1896. 
W.  Withering  :  An  Account  of  the  Foxglove,  Birmingham,  1785. 


CHAPTER  XXVII 
ACUTE    PERICARDITIS 

Pericarditis  is  less  common  than  endocarditis,  and  only- 
occurred  in  158  of  3,842  cases  who  were  admitted  to  hospital 
on  account  of  heart  disease;*  but  its  high  mortality  (63  of 
the  158  patients  died  during  their  residence)  makes  it  an  im- 
portant cause  of  death  in  cardiac  diseases. 

The  Lesions. — ^Pericarditis  may  be  local  or  diffuse,  and  may 
be  acute  or  chronic.  It  may  be  due  to  many  micro-organisms, 
the  pyogenic  cocci,  the  pneumococcus,  and  the  organism  of 
acute  rheumatism,  being  those  which  are  most  frequently 
causal;  while  a  tubercular  infection  is  by  no  means  uncommon, 
both  as  a  major  and  as  a  terminal  event.  In  the  acute  stage 
the  exudate  may  be  sero- fibrinous,  purulent,  or  haemorrhagic. 
If  recovery  ensues,  resolution  may  be  complete;  but  it  is 
usually  imperfect,  and  organization  of  the  exudate  occurs,  with 
adhesion,  partial  or  universal,  of  the  visceral  and  parietal 
layers. 

In  the  earliest  stage  the  serous  surface  is  hypersemic,  dull, 
and  opaque,  and  minute  haemorrhages  may  be  apparent  in  the 
vicinity  of  the  vessels,  with  here  and  there  a  few  flakes  of 
fibrin.  In  the  majority  of  cases,  however,  a  fibrinous  or  fluid 
exudation  is  found  on  examination.  The  fibrinous  exudate 
varies  in  character  in  different  cases.  It  may  be  scanty  and 
slight,  and  situated  mainly  around  the  great  vessels ;  or  thin 
and  more  diffuse,  covering  the  greater  part  of  the  heart  wq,ll ; 
or  abundant  and  universal,  involving  both  the  parietal  and 
the  visceral  layers.  The  deposit  is  usually  thickest  in  the 
vicinity  of  the  coronary  vessels.  From  the  constant  move- 
ment  of  the  heart  its  surface  is  rarely  smooth,  generally  pre- 

*  Lockhart  Gillespie ;  Grant  Andrew. 

385  25 


386  DISEASES  OF  THE  HEART 

senting  a  "rippled,"  honeycomb,  or  shaggy  appearance, 
with  bands  of  varying  thickness  here  and  there  uniting  the 
two  layers.  In  exceptional  cases  little  fluid  is  effused,  but  as 
a  rule  the  sac  contains  a  few  ounces,  even  in  those  cases  in 
which  the  fibrinous  deposit  is  most  extensive  and  thick.  In 
other  cases  the  fluid  effusion  is  considerable,  and  may  amount 
to  several  pints,  and  the  fibrinous  exudate  is  relatively  scanty. 
The  fluid  is  yellowish-green  in  colour,  and  generally  fairly 
clear,  but  it  may  be  turbid.  The  specific  gravity  is  about 
1-018,  much  albumin  is  present,  and  clotting  takes  place 
if  the  fluid  is  allowed  to  stand.  In  severe  infections  the  fluid 
may  be  frankly  purulent,  and  it  is  occasionally  hsemorrhagic 
in  character,  particularly  in  tubercular  cases.  In  the  slighter 
infections  the  exudation  may  be  completely  absorbed,  but  in 
the  majority  of  cases  adhesions  form  between  the  two  surfaces, 
and  are  ultimately  organized.  In  some  cases  calcareous 
material  is  deposited  between  the  two  layers. 

In  most  cases  the  chief  deposit  occurs  on  the  visceral  peri- 
cardium, and  the  pericardial  sac  is  but  slightly  involved ;  but 
in  others  the  parietal  layer  is  primarily  or  chiefly  involved, 
and  in  this  case  the  inflammation  may  extend  outwards  into 
the  mediastinum,  and  not  infrequently  involves  the  pleural 
sacs  as  well.  In  a  few  cases  the  primary  focus  is  without  the 
sac,  and  a  comparable  lesion  occurs,  but  with  a  different 
sequence.  Tubercular  pericarditis  sometimes  arises  in  this 
way  by  extension  from  infected  mediastinal  glands. 

In  acute  pericarditis  the  superficial  muscle  cells  may  be 
seriously  damaged,  showing  distinct  fatty  or  other  changes ; 
but  the  connective  tissue  of  the  heart  is  Httle  altered.  The 
fibrous  tissue  around  the  main  vascular  trunks  or  the  super- 
ficial layers  of  muscle  cells  may  be  more  bulky  than  normal, 
and  more  thickly  nucleated;  but  even  this  is  rare,  and  in  any 
case  the  lesion  is  always  superficial.  In  adherent  pericardium 
a  similar  state  of  matters  is  the  rule,  and  I  have  only  twice 
seen  any  considerable  degree  of  fibrosis  in  the  heart  muscle. 
In  both  cases  it  was  patchy  in  distribution,  and  in  one  case 
there  was,  in  addition,  widespread  valvular  disease.  Myo- 
cardial lesions,  however,  are  probably  always  related  to  causes 
other   than   the  pericarditis.     Acute   endocarditis   is   usually 


ACUTE  PERICARDITIS  387 

accompanied  by  a  varjdng  amount  of  myocarditis,  and  not 
infrequently  by  pericarditis  as  well;  and  a  myocardial  infarct 
or  abscess,  if  it  approaches  the  surface,  is  necessarily  associated 
with  pericardial  changes ;  but  these  are  the  result,  and  not  the 
cause,  of  the  myocardial  lesion.  In  tubercular  pericarditis, 
too,  the  superficial  muscular  layers  alone  are  usually  involved. 

In  mural  endocarditis,  on  the  other  hand,  the  muscle  is 
always  deeply  involved,  as  the  infection  spreads  outwards 
along  the  lymphatic  channels.  In  pericarditis  the  inflamma- 
tion does  not  travel  far  against  the  lymphatic  stream. 

The  milk  spots  which  are  so  often  seen  are  always  superficial, 
and  never  invade  the  muscle.  It  seems  probable  that  they 
are  rarely  the  result  of  acute  local  pericarditis.  They  are 
most  common  in  elderly  persons,  and  are  rare  in  childhood. 
They  are  generally  situated  on  the  front  of  the  heart  on  the 
parts  which  are  directly  related  to  the  sternum  and  ribs,  and 
are  unusual  on  the  parts  which  are  covered  by  the  lungs ; 
they  are  probably  due  to  mechanical  irritation  produced  by 
the  movements  of  the  heart  against  the  unyielding  bony 
thorax. 

The  functions  of  the  pericardia]  sac  are  frequently  gravely 
injured.  In  the  acute  stages  it  is  infiltrated  and  thickened 
by  inflammatory  exudate,  and  its  strength  and  resilience  are 
seriously  affected  if  it  is  at  this  stage  distended  by  effusion; 
and  they  are  still  more  disturbed  if  the  inflammation  spreads 
outwards  into  the  mediastinal  structures,  and  adhesions  form 
between  it  and  the  thorax  or  the  neighbouring  viscera. 

The  adhesions  which  follow  acute  pericarditis  vary  consider- 
ably in  distribution  and  in  site.  They  may  be  delicate,  tenuous, 
and  long,  or  dense  and  thick,  and  then  usually  short ;  and  while 
they  are  as  a  rule,  even  when  considerable,  more  or  less  localized, 
they  may,  in  exceptional  cases,  be  universal,  and  obHterate 
the  pericardial  cavity.  Complete  obliteration  of  the  sac  is 
unusual,  but  it  is  often  divided  into  several  compartments. 

Adhesions  may  be  present  anywhere,  and  may  interfere 
with  the  proper  action  of  the  heart,  as  they  may  embrace  and 
strangle  the  vense  cavse  and  the  right  auricle,  or  the  pulmonary 
veins  and  the  left  auricle ;  or  involve  the  aorta,  the  puhnonary 
iirtery,  or  the  ventricles. 


388 


DISEASES  OF  THE  HEART 


If  the  inflammation  spreads  outside  the  sac,  the  pericardium 
may  become  fixed  to  neighbouring  structures — the  sternum 
and  adjacent  ribs  in  front,  the  diaphragm  below,  the  lungs 
on  either  side,  or  the  vertebral  column  behind. 

The  Etiology  of  Acute  Pericarditis.  —  Pericarditis  may  be 
associated  with  man}-  diseases,  and  is  rare  as  a  primary  event.  It 
occurs  in  ( 1 )  the  infections  generally,  in  particular  acute  rheuma- 
tism; (2)  intrathoracic  disease  of  various  kinds;  (3)  general 
and  local  sepsis ;  and  (4)  chronic  disease,  as  a  terminal 
event. 

1.  Of  all  the  infections  acute  rheumatism  is  that  with  which 
pericarditis  is  most  frequently  associated,  and  its  incidence 
in  this  disease  is  considerable  (16  per  cent.),  though  decidedly 
less  than  that  of  endocarditis,  by  which,  however,  it  is  com- 
monly accompanied.  It  is  almost  equally  frequent  in  the  two 
sexes,  and,  like  endocarditis,  is  much  more  common  in  early 
life,  and  was  present  in  94  out  of  100  cases  of  fatal  heart 
disease  observed  by  Sturges*  at  Ormond  Street.  It  is  generally 
considered  to  be  most  usual  in  first  attacks  of  rheumatism,  but 
in  Church's  series,  56  per  cent,  occurred  in  second  or  subsequent 
attacks.  Its  incidence  is  greater  the  more  severe  the  arthritis, 
and  it  rarely  obtains  in  those  trivial  rheumatic  illnesses 
with  which  endocarditis,  on  the  other  hand,  is  so  often 
associated.  I 

*  Lancet,  1894,  vol.  i.,  pp.  583,  653,  723. 

t  The  Incidence  of  Pericarditis  in  Acute  Rheumatism  (Garrod). 


Acute 
Rheumatism. 

Pericarditis. 

Case 

Cases. 

Latham^ 

136 

18 

Peacock^ 

233 

36 

Sibson^          

326 

63 

Pye  Smith* 

400 

96 

Whipham^     . . 

655 

111 

OslerS             

Totals         

330 

2,080 

20 

344 

Church:  Of  155  cases  of  pericarditis  occurrmg  in  acute  rheumatism,  67 
accompanied  the  first  attack. 

{For  continuation  of  note,  see  next  'page.) 


ACUTE  PERICARDITIS  389 

Roberts  stated  that  it  is  not  uncommon  between  the  third 
and  the  sixth  day  of  the  arthritis.  Balfour  thought  that  the 
majority  of  cases  occurred  within  the  first  week;  and  in 
Sibson's  series*  the  signs  were  recognized  within  eleven  days 
in  nearly  haK  the  cases  (30  out  of  63  cases).  But  in  exceptional 
instances  the  onset  may  be  delayed  indefinitely,  as  late  as  the 
sixtj^-first  day  (Sibson),  or  may  supervene  during  a  relapse. 
A  married  woman,  aged  twenty-seven,  was  admitted  to  hospital 
suffering  from  acute  rheumatism  on  February  23.  The 
arthritis  soon  subsided,  but  on  March  20  a  consolidation 
appeared  at  the  base  of  the  left  lung.  In  the  early  part  of 
April  crops  of  subcutaneous  nodules  appeared,  and  on  the 
29th — two  months  after  the  subsidence  of  the  arthritis — 
pericarditis  was  recognized.  A  girl,  aged  fifteen,  suffered 
from  acute  rheumatism  in  December,  1910,  chorea  in  April  and 
June,  1911,  acute  rheumatism  in  November,  1911,  and  slight 
arthritis  for  a  few  days  in  January  and  April,  1912.  With 
the  last  attack  a  pericardial  effusion  developed.  In  both  of 
these  patients  acute  endocarditis  co-existed,  and  in  the  latter 
case  the  cardiac  infection  seemed  to  be  persistent  and  re- 
sponsible both  for  the  recurring  attacks  of  arthritis  and  the 
pericardial  infection. 

C^Aorea  is  responsible  for  many  cases  of  pericarditis.  In  Sibson's 
series  it  occurred  in  15  out  of  21  cases  of  acute  rheumatism 
which  were  associated  with  chorea.  Osier  found  that  it  was 
present  in  19  of  73  cases  of  chorea  examined  post-mortem  ;  and 
Cheadlef  has  drawn  attention  to  its  association  with  the  other 

{Continuation  of  notz  ("f")  on  previous  page.) 


Male.              Female. 

Church^        

Lockhart  Gillespie . . 
Sibson          . . 

12-22%         10-53'/        -2.2  90  Cttsv.3 
68                 51 
35        '         28 

! 

^  Quoted  by  A.  E.  Garrod.     A  Treatise  on  Rheumatism,  1890. 

2  Hem.  3  Log.  cit.  *  Quoted  by  Garrod.  ^  idem. 

^  "  The  Principles  and  Practice  of  Medicine,"  1912. 

''  AUbutt's  "  System,"  1 906,  vol.  ii.,  part  i.,  p.  594. 


*  Reynolds's  "System,"  1877,  vol.  iv.,  p.  186. 

f  "  Occasional  Lectures  on  the  Practice  of  Medicine,"  1900. 


390  DISEASES  OF  THE  HEART 

rheumatic   manifestations — erythema,   subcutaneous   nodules, 
and  tonsillitis. 

Pericarditis  is  of  rare  occurrence  in  the  other  infections. 
It  is  most  common  in  pneumonia  (1-2  per  cent.),  scarlatina 
(0-65  per  cent.),  and  enteric  fever  (0-2  per  cent.),  and  may 
occasionally  obtain  in  smallpox,  measles,  influenza,  diphtheria, 
and  gonorrhoea.  In  smallpox  it  is  probabty  due  as  a  rule  to 
a  secondary  infection.* 

2.  The  incidence  of  pericarditis  in  thoracic  disease  is  chiefiy 
due  to  its  association  with  pneumonia,  pleuris}^,  and  phthisis. 
Its  occurrence  in  pneumonia  is  of  serious  significance,  as  its 
post-mortem  incidence  (12-6  per  cent.)  is  much  greater  than 
that  reported  from  the  wards  (1-2  per  cent.).  It  is  uncommon 
in  pleurisy,  save  in  empyema.  In  phthisis  it  was  found  post- 
mortem in  4' 6  per  cent.  Some  cases  were  not  tuberculous? 
but  were  due  to  a  secondary  pyogenic  infection. 

It  may  follow  inflammatory  lesions  in  the  sternum,  ribs, 
or  mediastinal  glands,  whether  tubercular  or  pyogenic;  frac- 
tures of  the  ribs  and  perforating  wounds  of  the  thorax;  and 
rarely  inflammatory  lesions  below  the  diaphragm,  such  as  a 
perforated  gastric  ulcer  with  subphrenic  abscess. 

3.  Pericarditis  is  sometimes  a  terminal  event  in  pycemic 
cases.  It  may  then  be  secondary  to  a  myocardial  abscess,  or 
occur  apart  from  cardiac  disease,  as  the  result  of  a  direct 
blood  infection. 

4.  Pericarditis  is  not  uncommon  as  a  terminal  event  in 
chronic  diseases  of  various  kinds,  the  inflammation  occurring 
on  account  of  the  lessened  resistance  to  infection.  It  has  been 
met  with  in  anaemia,  cancer,  gout,  and  renal  disease,  and  is 


Pneumonia 

Post-mortem  series  (Musser  and  Norris)^ 

Scarlatina  (McCollum)- 

Enteric  fever  (McCrae)^  . . 

Phthisis  {posl-mortem  series)  (Norris)*  . , 


Cases. 

Pericarditis. 

Percent. 

40,773 

499 

1-2 

2,128 

267 

12-6 

2,000 

13 

0-65 

1,500 

3 

0-2 

1,780 

81 

4-6 

1  Osier's  "  System,"  1907,  vol.  ii.,  p.  537. 

2  Ihid.,  p.  334.  3  lud.,  p.  70. 

*  Quoted  by  Lawrason  Brown,  ibid.,  1908,  vol.  iii.,  p.  321. 


ACUTE  PERICARDITIS 


391 


most  common  in  the  latter,  in  particular  in  renal  cirrhosis, 
while  it  is  comparatively  rare  in  acute  nephritis.*  The  micro.- 
organisms  concerned  are  chiefly  the  pyogenic  cocci,  but  a 
tubercular  infection  is  by  no  means  rare. 

The  actual  incidence  of  these  factors  varies  in  different 
series,  mainly  on  account  of  variations  in  the  class  of  case 
under  observation;  but  the  most  common  accompaniment  is 
endocarditis,  which  is  usually  of  rheumatic  origin.  In  my 
series  of  30  cases  of  acute  endocarditis,  pericarditis  occurred 
in  4.  In  pneumonia,  pericarditis  is  usually  trivial,  and  merely 
terminal — an  indication  of  a  general  septicaemia;  but  it  may 
occur  early,  and  be  severe.  In  only  one  of  my  cases  was  it 
considerable,  the  exudation  being  mainly  fibrinous,  and  due  to 
the  pneumococcus,  fthough  gonococci  were  present  in  an 
urethral  discharge,  and  the  bacillus  of  diphtheria  in  the 
throat  !  Of  the  cases  associated  with  renal  disease,  one  was 
due  to  a  tubercular  infection,  and  one  of  those  accompanying 
tuberculosis  was  caused  by  a  streptococcus. f 

The  Symptoms  o£  Pericarditis. — ^The  symptoms  of  acute 
pericarditis  vary  considerably  in  different  cases,  as  they  may 
arise  in  various  ways .  In  the  early  stages  and  in  small  effusions 
the  interference  with  the  cardiac  action  is  shght,  but  in  large 

*  PosT-MoETEM  Statistics. 


Nephritis. 

Amyloid  Kidney. 

Cirrhotic  Kidney. 

[Cases. 

Pericarditis. 

Cases. 

Peri- 
carditis. 

Cases. 

Peri-     ' 
carditis. 

Dickinson^  .. 
Grainger- 

Stewart^ 

Sibson^ 

39 

28 

2-5% 
7-0% 

48 
50 

22 

6-2% 
8-0% 

9-0% 

68 
13 

162 

23-5% 

7-5% 

14-1% 

1 

Acute 
Nephritis. 

Chronic 
Nephritis. 

Cases. 

Peri- 
carditis. 

^^^®-     carditis. 

21 

19-0% 

62        9-6% 

^  "Diseases  of  the  Kidney."      London,  vol.  ii.,  1877. 
2  "Diseases  of  the  Kidneys."     Edinburgh,  1871. 

f  See  footnote  (a)  on  page  392 


3  Loc.  cit. 


392 


DISEASES  OF  THE  HEART 


efihisions  the  mechanical  interference  is  considerable.  The 
amount  of  fluid  may  be  large  (as  much  as  a  gallon,  Gibson), 
and  much  greater  than  a  normal  pericardium  can  hold  (less 
than  1|  pints) ;  and  although  an  inflamed  pericardium  stretches 
under  the  strain,  the  pressure  within  the  sac  always  rises. 
Starling*  has  observed  the  results  in  experiment.  On  intro- 
ducing oil  into  a  dog's  pericardium,  the  venous  pressure 
steadity  rose,  though  the  aortic  pressure  at  first  remained 
constant ;  but  a  critical  point  was  soon  reached  when  the  intra- 
pericardial  pressure  rose  to  such  a  height  that  it  prevented 
the  diastohc  filling  of  the  heart,  and  the  supply  of  blood  to 
the  ventricles  failed.  The  pulse  then  became  small,  and  the 
blood-pressure  rapidly  fell. 

The  increasing  difficulties  can  be  readily  observed  during 
the  stage  of  an  increasing  effusion,  the  pulse-rate  becoming 
more  frequent,  and  the  volume  and  pressure  lessening, 
while  the  surface  becomes  cyanosed  and  the  respirations  diffi- 
cult. Hepatic  engorgement  is  usual,  but  oedema  is  uncommon 
and  is  rarely  extensive. 

Pericardial  inflammation  has   little  direct   effect  upon  the 


(a)  For  reference  to  this  footnote  see  f  in  text  on  page  391. 


Hirschfelderi     | 
(Johns  Hopkins  '     Personal. 
Hospital). 


Endocarditis 

53 

Mvocarditis 

8 

Pneumonia 

39 

Acute  rheumatism 

31 

Xephritis 

33 

Tuberculosis 

25 

Pleurisy  . . 

17 

Gonorrhoea 

3 

Aneurism 

2 

Leukaemia 

2 

'   Syphilis  . . 

1 

Sepsis 

Totals 

— 

214 

28 


142 
53 
1 


59* 


"  Diseases  of  the  Heart  and  Aorta." "    Philadelphia,  1910. 

One  -was  tubercular.  ^  Q^e  -was  pyogenic. 

In  17  of  these  cases  the  patients  had  suffered  from  acute  rheumatism. 


Lancet,  1897,  vol.  i.,  pp.  569,  652,  723. 


ACUTE  PERICARDITIS  393 

cardiac  muscle,  and  lesions  which  are  found  post-mortem  in 
uncompKcated  cases  are  always  trivial  and  confined  to  the 
superficial  muscular  layers.  But  pericarditis  is  rarely,  if  ever, 
uncomplicated.  Endocardial  lesions  are  often  present,  and  a 
m^yocarditis  not  infrequently  co-exists.  Pleural  or  pulmonary 
d'sease  may  originate  or  accompany  the  pericardial  inflam- 
mation. 

The  pericardium,  too,  is  situated  within  the  thorax,  whose 
walls  are  capable  of  only  limited  displacement,  and  an  increase 
in  its  size  can  only  be  accommodated  by  pressure  upon  the 
neighbouring  viscera.  The  lungs  are  compressed  and  emptied 
of  their  air,  the  oesophagus  is  driven  against  the  vertebrae,  the 
superior  vena  cava  is  obstructed,  and  the  vagus,  phrenic  or 
recurrent  laryngeal  nerves  may  be  implicated,  and  the  symp- 
toms in  different  cases  vary  accordingly. 

The  onset  of  pericarditis  is  more  frequently  attended  by  the 
occurrence  of  definite  symptoms  than  is  the  case  in  endocar- 
ditis, and  they  general^  suggest  a  cardiac  origin;  but  peri- 
carditis may  be  latent  and  only  recognized  on  routine  examina- 
tion or  post-mortem.  This  is  most  likely  to  happen  when  the 
patient  is  already  seriously  ill  and  insensitive  to  trivial  dis- 
comforts, or  in  cases  where  a  pulmonary  affection  interferes 
with  auscultation;  but  even  in  subacute  rheumatism  it  may 
be  latent.  A  boy,  aged  eighteen,  who  was  resident  in  my 
wards  on  account  of  an  attack  of  acute  rheumatism,  suffered 
from  a  relapse  of  the  arthritis  of  short  duration  and  sKght 
severity,  and  typical  friction  sounds  and  enlargement  of  the 
area  of  cardiac  dulness  were  discovered  on  routine  examina- 
tion of  the  chest,  though  the  pulse-rate  remained  unaltered, 
and  no  thoracic  discomfort  was  experienced. 

In  about  half  the  cases  (15)*  the  patient  complains  of 
discomfort  or  pain  over  the  front  of  the  chest.  The  pain  is 
rarely  severe,  and  may  be  general  or  referred  to  the  base  or 
to  the  xiphoid  cartilage,  and  varies  in  intensity  at  different 
times  without  any  obvious  cause.  It  is  less  frequent  and  less 
severe  in  dry  pericarditis  than  in  cases  with^effusion ;  and  if 

*  The  figures  in  brackets  show  the  incidence  of  symptoms  in  a  series  of 
30  cases. 


394  DISEASES  OF  THE  HEART 

present  in  the  early  stages,  may  become  more  marked  or  may 
remit  with  the  occurrence  of  effusion.  If  the  effusion  is  con- 
siderable, some  complaint  is  almost  invariable,  and  occasion- 
ally the  anguish  is  extreme.  The  pain  is  generally  increased 
by  pressure  with  the  stethoscope,  but  this  probably  depends 
upon  the  mobihty  of  the  chest  wall,  and  is  more  constant  in 
children  than  in  elderly  persons  with  calcified  costal  cartilages. 
In  some  cases  the  pain  on  pressure  is  due  to  tenderness  of  the 
skin,  and  even  the  slightest  pressure  with  the  stethoscope  is 
resented,  and  poultices  and  fomentations  cannot  be  borne ;  but 
this  is  exceptional.     Palpitation  is  not  uncommon. 

The  pulse  is  ahnost  always  affected.  In  the  early  stages  it 
is  more  frequent  than  normal,  and  out  of  proportion  to  the 
degree  of  fever.  With  the  onset  of  effusion  the  rate  increases 
and  the  volume  and  pressure  diminish  in  corresponding  degree 
to  the  pressure  exercised  upon  the  heart.  The  pulsus  para- 
doxus may  be  present,  but  seldom  in  characteristic  degree. 
The  rhythm  of  the  heart  has  never,  in  my  experience,  altered, 
though  irregularities  have  often  been  described.  Pericarditis 
is  generally  met  with  in  cases  where  other  lesions  co-exist,  and 
frequently  occurs  in  persons  whose  pulse  is  already  irregular, 
so  that  extra-systoles,  auricular  fibrillation,  etc.,  are  not  rare; 
but  these  are  seldom,  if  ever,  the  result  of  the  pericardial 
inflammation. 

Shortness  of  breath  is  quite  as  frequently  present  (18)  as 
prsecordial  pain.  It  may  of  course  be  due  to  associated 
pulmonary  or  pleural  disease,  but  it  occurs  also  in  uncomph- 
cated  cases.  It  is  never  extreme  in  cases  without  effusion,  and 
is  usually  severe  in  corresponding  degree  to  the  amount  of 
fluid,  and,  if  this  is  considerable,  ma3^  be  accompanied  by 
orthopnoea  (11).  Sometimes  the  breathlessness  is  paroxysmal 
and  occurs  mainly  at  night,  or  is  of  the  Cheyne-Stokes  type; 
but  this  is  probably  always  due  to  accompanying  renal  disease, 
which  was  present  in  the  3  cases  of  this  series  in  which  it  was 
observed. 

The  other  symptoms  which  may  be  present  are  all  less  con- 
stant. The  facial  aspect  may  be  changed,  the  countenance 
becoming  anxious  and  unduly  pale  (2),  or  distinctly  cyanosed 
(9).     This  is  most  usual  in  effusion,  and  the  degree  of  cyanosis 


ACUTE  PERICARDITIS  395 

in  particular  may  be  taken  as  an  index  of  the  degree  with  which 
the  effusion  is  interfering  with  the  cardiac  work. 

Difficulty  in  swallowing  (1)  or  choking  attacks  (1)  may  be 
present  in  cases  where  the  effusion  is  large  and  presses  upon 
the  oesophagus.  The  difficulty  is  usually  increased  if  the 
patient  is  recumbent,  and  is  reheved  by  the  erect  position. 
The  voice  may  become  weak  and  lost  if  the  laryngeal  nerves 
are  specially  impHcated.  The  veins  of  the  neck  may  be  turgid 
and  distended,  and  the  face  and  head  may  be  swollen  and 
puffy.  The  systemic  veins,  too,  may  be  congested;  but 
oedema  (1)  is  rarely  extensive.  Hepatic  enlargement  may  be 
distinct,  and  accompanied  by  tenderness  on  pressure  in  the 
epigastrium. 

In  serious  cases  the  patients  are  drowsy,  or  restless  and 
sleepless,  and  are  often  mildly  dehrious  at  night.  Acute  cere- 
bral symptoms  occasionally  ensue.  Fever  is  inconstant.  In 
acute  rheumatism  the  temperature  rises  on  the  onset  of  peri- 
carditis, but  the  rise  may  be  inconsiderable  and  hyperpyrexia 
is  rare.  In  renal  cases  and  in  terminal  pericarditis  fever  is 
generally  shght  or  absent. 

The  course  of  events  in  an  attack  of  pericarditis  varies  greatly 
in  individual  cases,  for  the  causal  factors  differ  widely,  and  it 
may  be  a  minor  accompaniment  of  a  serious  ailment  in  which 
other  viscera  are  gravely  involved,  or  the  chief  episode  of  a 
purely  cardiac  iUness.  In  pneumonia,  for  example,  peri- 
carditis is  generally  merely  an  indication  of  a  widespread 
septicaemia  and  an  additional  cause  of  cardiac  strain;  in 
pyaemia  it  is  but  an  item  in  a  widespread  sepsis ;  and  in  renal 
disease  an  indication  of  the  way  in  which  death  is  approaching, 
rather  than  its  cause.  In  all  three  cardiac  weakness  is  often 
present,  and  the  advent  of  the  serous  inflammation  merely 
accentuates  the  pre-existing  symptoms,  and  it  is  apt  to  be 
missed  unless  routine  examinations  are  frequently  made.  Even 
in  the  cardiac  group  associated  with  acute  rheumatism  its 
effects  are  often  indistinct,  for  endocarditis  and  myocarditis 
may  co-exist,  and  the  exact  influence  of  each  factor  can  rarely 
be  measured.  The  amount  of  the  effusion  cannot  be  accurately 
gauged  by  the  size  of  the  area  of  cardiac  dulness,  for  this  may 
be  enlarged  from  hypertrophy  consequent  upon  a  valvular 


396 


DISEASES  OF  THE  HEART 


flaw,  from  dilatation  on  account  of  loss  of  tone,  or  from  the 
presence  of  effusion,  or  maj-  be  tlie  sum  total  of  all  three  factors. 
In  the  majorit}'  of  cases  the  sj-mptoms  are  only  in  part  due  to 
the  pericarditis,  their  character  is  necessarity  inconstant,  and 
their  progress  varies  within  wide  limits. 

The  anatomical  distinctions  between  dry  pericarditis,  effu- 
sion, and  adhesion  are  also  onty  accurate  in  a  general  way, 
and  everj'  case  does  not  run  the  full  course.  Friction  may  be 
audible  for  days  without  the  occurrence  of  slitv  appreciable 
effusion,  and  in  a  man,  aged  seventy-two,  who  died  in  my 
wards  from  bronchitis  and  renal  cirrhosis,  it  was  constantly 
present  from  February  22  until  April  9,  while  the  pericardial 
sac  on  ■post-mortem  examination  only  contained  4  ounces  of 
fluid.  Fluid  may  be  poured  out  rapidly,  and  within  three  or 
four  days  exert  an  obvious  mechanical  influence  upon  the 
cardiac  action,  or  maj^  appear  and  disappear  insidiously  and 
gradually — results  which  must  be  due  to  variations  in  the 
virulence  of  the  bacterium  and  in  the  resistance  of  the  indi- 
vidual. The  effusion  in  rheumatic  cases  is  usually  sero- 
fibrinous and  rarely  purulent;  in  tubercular  cases,  in  cancer, 
and  in  scurv\%  it  is  often  hsemorrhagic ;  and  pus  is  likely  to 
occur  in  streptococcic  infections.  And  while  a  purulent  effu- 
sion generally  terminates  fatally,  as  in  the  comparable  empy- 
ema, unless  operative  interference  is  successfulh'  undertaken, 
the  recoveries  which  occasionally  ensue  in  the  latter  disease 
suggest  that  a  similar  result  maj^  obtain  in  purulent  pericar- 
ditis, a  suggestion  which  is  borne  out  by  the  discovery  in  a 
few  cases  of  cretaceous  material  within  the  sac. 

The  relative  frequency  of  the  various  forms  of  pericarditis 
is  indicated  by  the  following  table,  which  shows  their  incidence 
in  the  post-mortem  room : 


Sero-fibrinous 

. .      108* 

Hsemorrhagic 

..       30 

Purulent 

..       24 

Tubercular  (secondary) 

..24 

Tubercular  (primary) 

2 

Partially  adherent   . . 

'.      !!    Ill 

Totally  adherent 

..       23 

Ossified 

2 

324 

*  Breitung,  quoted  by  G.  A.  Gibson. 


1 


ACUTE  PERICARDITIS  397 

In  acute  rheumatism  the  onset  of  pericarditis  is  most  usually 
rapidly  followed  by  effusion,  which,  within  a  few  days  (as  a 
rule  three  or  four,  rarely  a  week)  attains  a  maximum,  and 
then  gradually  disappears.  The  process  can  be  followed  more 
or  less  accurately  from  day  to  day  by  percussion,  the  area  of 
dulness  steadily  increasing  and  then  lessening.  Considerable 
differences,  however,  occur  in  the  duration  of  the  effusion.  In" 
a  few  cases  the  area  of  cardiac  dulness  regains  its  normal  hmits 
within  a  fortnight,  but  in  others  not  for  many  weeks.  An 
exudate,  which  is  mainly  serous,  is  rapidly  removed,  but  a 
thick  fibrinous  deposit  necessitates  the  formation  of  granula- 
tion tissue,  and  months  may  elapse  before  any  appreciable 
alteration  in  the  area  of  cardiac  dulness  can  be  detected.  In 
a  large  majority  of  cases  recoverj-  ensues  spontaneously,  unless 
the  endocardial  lesions  are  widespread  and  actively  pro- 
gressive. 

Sir  Wilham  Osier  states  that  dry  pericarditis  does  not  kill, 
though  it  frequently  occurs  in  dying  patients,  and  the  dictum 
is  probably  accurate.  In  effusion,  too,  the  actual  mortality 
is  probably  small,  and  the  gravity  of  the  individual  prognosis 
depends  chiefly  upon  the  amount  of  the  effusion  and  the  degree 
of  pressure  exercised  upon  the  heart;  but  I  have  only  seen 
three  or  four  cases  in  which  death  seemed  to  result  in  this  way. 
The  mortality  of  pericarditis,  however,  is  great  (39-8  per  cent., 
G.  A.  Gibson),  so  that  its  advent  is  always  a  herald  of  evil 
omen,  even  though  it  only  acts  indirectly. 

In  exceptional  cases  pericarditis  is  chronic,  or,  at  any  rate, 
subacute.  The  duration  of  the  illness  is  prolonged,  and  on 
2?05^-mor^em  examination,  a  soft,  succulent  exudation  is  found 
loosely  uniting  the  two  layers.  In  tubercular  cases,  too,  the 
progress  may  be  subacute,  and  much  caseous  matter  may  be 
found,  the  parietal  and  visceral  layers  being  separated  at  times 
by  half  an  inch  of  caseous  material. 

The  Physical  Signs  oS  Pericarditis. — ^In  fibrinous  pericarditis 
the  characteristic  friction  may  be  felt  hj  the  hand,  but 
it  is  usually  only  apparent  on  auscultation.  The  sounds 
are  superficial,  and  seem  to  originate  close  to  the  ear. 
They  are  usually  double  (to  and  fro)  and  of  cardiac 
rhythm,  but  they  do  not  correspond  closely  to  the  cardiac 


398  DISEASES  OF  THE  HEART 

movements  or  sounds,  occurring  a  little  after  systole  has 
commenced,  and  continuing  till  a  short  period  before  the 
cessation  of  diastole,  with  an  interval  between  the  systohc  and 
the  diastohc  portion,  and  covering  rather  than  replacing  the 
cardiac  sounds.  The  sounds  may  be  of  varying  quality — very 
soft,  or  harsh  and  grating,  or  scratching,  or  creaking  Hke  the 
creaking  of  new  leather.  The  systohc  element  is  usuallj^ 
louder  and  longer  than  the  diastolic.  Sometimes  the  sound  is 
single  and  systolic  in  rhythm,  and  it  may  be  triple  if  the 
auricular  contractions  impart  a  special  emphasis  at  the  end 
of  ventricular  diastole.  The  friction  is  usually  loudest  be- 
tween the  apex  and  the  xiphoid  cartilage,  and  may  be  audible 
all  over  the  cardiac  area  and  even  a  little  beyond  it,  or  may 
be  hmited  to  a  small  area.  It  is  occasionally  only  audible 
towards  the  base,  or  more  rarely  at  the  apex.  It  is  variable 
in  its  distribution  and  character,  which  may  change  from  day 
to  day.  It  is  often  intensified  by  pressure  with  the  stethoscope 
over  an  interspace  and  by  alterations  in  the  respiratory  phases, 
but  it  may  be  loudest  during  either  inspiration  or  expiration; 
it  may  be  unaffected.  The  sounds  may  vary  in  character 
and  site  with  changes  in  position.  There  are  no  lines  of  con- 
duction outwith  the  cardiac  area,  as  in  aortic  valvular  disease, 
and  the  sound  is  rapidly  lost  when  the  cardiac  borders  are 
transgressed. 

There  is  as  a  rule  little  diflficulty  in  recognizing  the  nature 
of  the  sounds.  They  may  resemble  the  murmurs  of  double 
aortic  disease,  but  these  are  constant  in  character  and  site,  and 
are  conducted  in  definite  directions.  Pleuro-pericardial  fric- 
tion rarely  occasions  difficulty.  It  occurs  when  the  pleural 
spaces  overlving  the  heart  are  involved,  when  the  friction  may 
be  cardiac  in  rhythm;  but  full  inspiration  or  full  expiration 
almost  always  abolishes  the  sounds,  while  in  pericarditis  the 
friction  never  disappears,  even  though  the  respiratory  move- 
ments alter  its  quality.  It  is  only  audibly  at  the  periphery  of 
the  cardiac  area,  especially  about  the  upper  and  left  borders,  and 
it  is  generally  accompanied  by  evident  pleural  friction  elsewhere. 

Difficulty  may  be  experienced  when  the  sound  is  single,  but 
its  quality  may  be  characteristic,  and  its  variations  from  day 
to  day  separate  it  clearly  from  an  endocardial  murmur. 


ACUTE  PERICARDITIS 


399 


In  large  effusions  in  thin  persons  the  physical  signs  are 
distinct.  The  prgecordia  may  be  prominent  if  the  chest  wall 
is  soft,  and  the  interspaces  may  be  flush,  or  even  bulging 
above  the  ribs,  and  the  overlying  skin  may  be  cedematous. 
The  apex  impulse  becomes  weaker,  and  may  disappear, 
though  pulsation  may  be  apparent  in  the  fourth  interspace ; 
and  the  expansion  of  the  left  chest  on  inspiration  is  less  free 
than  that  of  the  right. 
The  movement  of  the  dia- 
phragm, too,  is  less  am- 
ple, in  particular  upon 
the  left  side,  and  the 
liver  and  spleen  may  be 
evidently  displaced 
downwards .  The  area  of 
cardiac  dulness  is  in- 
creased in  all  directions. 
The  upper  border  rises 
above  the  third  rib,  and 
may  extend  as  high  as 
the  fi.rst,  the  maximum 
elevation  being  over  the 
sternum.  The  left  border 
extends  outwards,  and 
may  be  an  inch  or  more 
beyond  the  apex  im- 
pulse, if  that  still  per- 
sists, and  the  right  border 
extends  towards  or  as 
far  out  as  the  right  nip- 
ple. The  shape,  too,  is 
altered,  and  it  is  conical  instead  of  rectangular,  the  maximum 
diameter  being  at  the  xiphoid  level  (Figs.  187,  188). 

The  fifth  right  interspace  is  encroached  upon  early,  and  the 
cardio-hepatic  angle  is  obtuse  instead  of  right-angled,  as  in 
enlargement  of  the  right  auricle.  The  friction  sounds  usually 
persist,  but  their  area  of  distribution  becomes  circumscribed. 
They  are  generally  audible  over  the  base  of  the  heart,  or 
rarely  at  the  extreme  apex;  but  they  are  sometimes  httle 


Pig.  187. — Diageajvi  showing  the  Shape  of 
THE  Area  of  Dulness  in  Pericardial 
Effusion. 


400 


DISEASES  OF  THE  HEART 


altered  if  the  heart  retains  its  relationship  with  the  front  of 
the  chest.  The  cardiac  sounds  become  weak,  muffled,  and 
indistinct,  and  in  large  effusions  may  be  short  and  very- 
distant. 

Some  other  signs  have  been  described,  but  their  occurrence 
is  occasional.  The  shoulder  girdle  may  be  raised,  so  that  the 
finger  can  be  introduced  between  the  left  clavicle  and  the  first 

rib  close  to  the  sternum. 
An  area  of  dulness,  with 
diminished  respiratory 
murmur,  may  be  found  at 
the  extreme  left  base  close 
to  the  vertebral  column, 
and  tubular  breathing, 
with  segophon}^,  may  be 
recognized  at  the  angle  of 
the  left  scapula. 

In    thin    subjects    the 

diagnosis     of     pericardial 

effusion  is    usually  made 

without  difficulty,  but  it 

may  be  difficult   in  very 

fat    people,    especially   if 

the  case  only  comes  under 

observation    at      a      late 

stage.     In  dilated  hearts 

pulsation  tends  to  become 

more  widespread,  though 

EiG.  188.— Diagram  showing  the  Shape  of    less  ample  and   of  shorter 

THE  Area  of  Dulness  in  Dilatation  of    duration,    rather    than    tO 

THE  Heart. 

disappear.     The    area    of 

dulness  is  increased  laterally  rather  than  upwards,  and  in  mitral 
stenosis  alone  reaches  as  high  as  the  second  rib,  unless  the  heart 
is  displaced  upwards  by  abdominal  distension ;  and  the  cardio- 
hepatic  angle  is  a  right  angle.  The  sounds  are  generally 
short  and  sharp  and  superficial,  and  are  often  loud  rather  than 
distant  and  indistinct.  The  liver  and  spleen,  though  fre- 
quently enlarged,  are  not  grossly  displaced. 

The  physical  signs  may,  however,  mislead.     As  a  rule,  with 


ACUTE  PERICARDITIS  401 

the  occurrence  of  effusion,  the  fluid  collects  between  the  heart 
and  the  front  of  the  chest,  so  that  the  apex  impulse  disappears, 
the  friction  area  diminishes,  and  the  sounds  become  distant. 
But  the  heart  may  retain  its  position  in  front,  while  the  fluid 
accumulates  elsewhere.  In  one  case  under  my  observation  a 
well-marked  apex  impulse  persisted  unchanged  during  the 
progress  of  an  effusion,  and  the  friction  area  remained  constant, 


Fig.  189. — Skiagram:  Pericarditis,  with  Effusion-  and  Left  Pneumothorax 

(J.  R.  K). 

as  the  apex  was  firmly  anchored  to  the  adjacent  pericardium 
by  a  thick,  short  band,  the  residue  of  an  antecedent  pericar- 
ditis. In  another  case  the  right  border  of  the  area  of  dulness 
remained  immobile  as  the  right  pleural  sac  was  obhterated 
and  adherent  to  the  chest  wall.  And  in  a  third  the  area  of 
dulness  diminished  in  size  and  moved  steadily  to  the  right 
side  from  the  gradual  development  of  a  left  pneumothorax, 

26 


402  DISEASES  OF  THE  HEART 

The  pulse,  too,  may  be  a  fallible  guide  to  the  degree  of  the 
effusion.  As  a  rule  it  steadily  becomes  more  frequent,  quick, 
and  soft ;  but  its  character  may  be  disguised  by  arterial  thicken- 
ing, aortic  regurgitation,  or  antecedent  high  blood-pressure. 
The  shape  of  the  distended  pericardium,  as  shown  in  a  skia- 
gram (Fig.  189),  is  characteristic;  but  examination  of  this  kind 
is  rarety  possible. 

The  onset  of  pericarditis  may  be  latent,  and  the  diagnosis 
may  be  made  on  routine  examination.  In  the  majority  of 
cases,  however,  complaint  of  pain  in  the  cardiac  region,  or 
an  exacerbation  of  the  fever,  attract  attention,  and  are  associ- 
ated with  an  increase  in  the  rate  of  the  pulse.  The  latter  is 
rarely  absent,  and,  as  in  acute  endocarditis,  the  pulse-rate  is 
increased  out  of  proportion  to  the  fever  and  the  number  of 
respirations,  the  pulse-respiration  ratio  becoming  5,  or  even  6, 
to  1.  With  the  occurrence  of  effusion,  the  pulse-rate  still 
further  increases,  the  respirations  become  more  frequent,  and 
the  extraordinary  muscles  of  respiration  are  brought  into  play, 
while  the  mucous  membranes  become  cyanosed,  and  the 
patient  is  forced  to  sit  up  in  bed.  With  an  increasing  effusion, 
the  distress  is  rapidty  augmented,  the  countenance  becomes 
anxious  and  distressed,  the  cyanosis  deeper,  and  the  pulse 
and  respirations  stiU  more  frequent.  In  the  later  stages 
the  cardiac  exhaustion  steadily  increases,  the  pulse  is  smaller 
and  more  quick  and  of  lessened  pressure,  the  cyanosis 
is  combined  with  an  ashen  pallor,  and  the  patient  tends  to 
sink  downwards  in  the  bed,  his  skin  often  bedewed  with  a  cold 
sweat,  and  death  ensues  from  cardiac  failure. 

In  the  individual  case  attention  should  be  paid  to  the  fea- 
tures which  have  just  been  mentioned.  The  occurrence  of 
orthopnoea,  unassociated  with  an}"  pulmonary  lesion,  a  definite 
diminution  in  the  volume  and  strength  of  the  pulse,  and  the 
combination  of  pallor  and  cyanosis,  are  all  of  evil  omen.  The 
degree  of  pyrexia  is  of  little  importance,  but  the  rate  of  the 
pulse  and  of  the  respirations  convey  their  special  lesson  of 
cardiac  or  respiratory  embarrassment.  Failure  to  maintain 
the  erect  posture,  if  unaccompanied  by  definite  evidence  of 
improvement,  is  a  most  serious  symptom. 


CHAPTER  XXVIII 
ADHERENT  PERICARDIUM 

The  term  "'adherent  pericardium  "  is  generalty  used  some- 
what loosely,  and  comprises  all  cases  in  Avhich  local  or  universal 
adhesions  exist  between  the  visceral  and  parietal  layers  of  the 
sac.  Mediastino-jDericarditis  includes  two  groups  :  one  in  which 
with  pericardial  adhesions  there  is  a  marked  increase  of  the 
fibrous  tissue  in  the  mediastinum,  with  adhesion  of  the  exterior 
of  the  pericardium  to  surrounding  parts  [indurative  mediastino- 
pericarditis) ;  and  a  second  in  which  with  pericardial  adhesions 
the  parietal  pericardium  is  adherent  to  surrounding  parts,  with 
little  or  no  general  mediastinitis  [pericarditis  interna  et  externa). 
Chronic  mediastinitis  implies  that  there  are  no  internal  peri- 
cardial adhesions. 

Pericardial  adhesions  necessarily  entail  additional  work  for 
the  heart,  but  this  may  be  insufficient  to  produce  appreciable 
hj^pertrophy  if  they  are  tenuous  and  lengthy  and  limited  in 
their  distribution,  and  Sibson*  collected  50  cases  in  which  the 
size  of  the  heart  was  normal.  If,  on  the  other  hand,  the  adhe- 
sions are  thick  and  extensive,  and  if,  in  addition,  they  extend 
outside  the  sac  and  fix  the  heart  to  adjacent  parts  and  limit 
its  free  movement,  hypertrophy  is  always  considerable  and  of 
appreciable  degree.  When  pericardial  adhesions  and  valvular 
disease  co-exist,  the  heart  is  alwa^-s  hypertrophied,  and  Sibson 
found  that  hearts  with  valvular  defects  and  adhesions  were  de- 
finitely heavier  than  hearts  in  which  comparable  valvular  defects 
were  present  without  adhesions  ;  so  that  the  latter  must  be  hedl 
responsible  for  some  part,  at  any  rate,  of  the  hypertrophy. 

Local  adhesions  are  most  frequently  found  at  those  parts  of 
the  heart  which  alter  their  relations  to  the  parietal  pericardium 
in  least  degree  during  the  cardiac  movements.  The}"  are  thus 
most  common  near  the  apex  and  about  the  left  border  of  the 

*  Loc.  cit. 
403 


404  DISEASES  OF  THE  HEART 

left  ventricle,  over  the  left  auricle,  and  at  the  basal  regions 
of  the  great  vessels ;  and  are  less  common  over  the  right 
ventricle,  the  right  auricle,  and  the  origins  of  the  great  vessels. 

The  extra-pericardial  adhesions  also  vary  in  their  site  and 
extent,  and  the  heart  may  be  adherent  to  the  lungs,  the 
diaphragm,  the  sternum  and  adjacent  ribs,  or  even  to  the 
vertebral  column.  The  inflammatory  spread  is  sometimes 
minimal  and  sometimes  local,  and  the  symptoms  and  signs 
correspond  accordingl^^  Pericardial  adhesions,  too,  may  vary 
in  their  effects  upon  the  different  chambers  of  the  heart.  They 
uiaiy  surround  and  entangle  the  auricles  and  great  veins  and 
hinder  the  influx  of  the  blood ;  or  embrace  the  ventricles  and 
the  arteries  and  impede  its  exit  from  the  heart.  If  the  pleural 
cavities  are  obliterated,  or  the  heart  is  adherent  to  the  parietes, 
the  respiratory  movements  will  affect  the  cardiac  action. 

The  etiology  of  adherent  pericardium  is  presumably  similar 
to  that  of  acute  pericarditis,  but  the  chronicity  of  the  affection 
makes  it  difficult  to  appreciate  the  various  factors  at  their 
proper  value.  In  Sibson's  series  49  out  of  80  cases  had  valvular 
lesions,  with  as  a  rule  some  form  of  chronic  renal  disease.  In 
3  cases  aneurism  of  the  aorta  was  present,  and  in  1  cancer  of  the 
heart.  In  19  cases  the  valves  and  aorta  were  health}-,  and  in 
7  of  the  19  no  other  viscus  was  diseased.  In  22  cases  which  I 
have  observed  13  had  valvular  disease,  of  whom  4  had  renal 
disease  in  addition;  and  in  9  the  valves  were  normal,  of 
whom  4  had  renal  lesions ;  4  cases  suffered  from  tuberculosis ; 
1  from  a  chronic  pulmonary  fibrosis,  which  probably  originated 
in  an  acute  pleuro-pneumonia  accompanied  by  empyema;  in 
1  the  origin  was  unknown,  as  it  was  discovered  in  a  patient  who 
died  from  acute  pneumonia ;  and  in  1  it  arose  during  acute 
rheumatism,  though  no  valvular  lesion  was  found  'post-7nortem. 

In  Harris's  series  of  cases  of  mediastino-pericarclitis  examined 
post-morte7n,  11  seemed  to  be  due  to  tuberculosis,  2  to  acute 
rheumatism  and  enteric  fever,  and  1  to  chronic  bronchitis, 
syphilis,  scarlatina,  and  trauma.  In  6  the  origin  was  not  ap- 
parent, and  the  symptoms  commenced  insidiously  without  am- 
obvious  acute  thoracic  disease. 

The  symptoms  in  adherent  pericardium  depend  upon  the 
amount  of  interference  with  the  cardiac  action  which  the  adhe- 


ADHERENT  PERICARDIUM  405 

sions  produce,  and  are  in  many  cases  absent  altogether,  as 
from  their  extent  or  from  their  character  they  do  not  incom- 
mode the  heart.  In  other  cases  the  interference  is  consider- 
able, but  the  co-existence  of  valvular  disease  in  sufficient 
degree  to  account  for  the  symptoms  which  are  present  makes 
the  recognition  of  the  pericardial  element  difficult  if  not  im- 
possible. So  that  in  the  majority  of  cases  the  condition  is  first 
recognized  post-mortem,  unless  the  previous  existence  of  an 
acute  pericarditis  is  already  known. 

In  cases,  however,  where  adhesions  exist  outside  the  peri- 
cardial sac,  as  well  as  within  it  (mediastino-pericarditis) 
symptoms  of  cardiac  insufficiency  are  generally  manifest,  as 
they  entail  a  very  considerable  amount  of  extra  work  on  the 
heart,  and  so  curtail  the  reserve  to  an  appreciable  degree. 
Sequeira  has  suggested  that  the  difficulties  may  originate  in 
another  way  from  that  which  has  been  already  discussed.  The 
pericardium  is  strong  and  indistensible,  and  under  normal  con- 
ditions prevents  undue  distension  of  the  cardiac  cavities  under 
the  stress  of  physical  exertion.  In  acute  pericarditis  its 
resistance  may  be  seriously  impaired  by  inflammation,  and  its 
cavity  may  be  grossly  distended  by  effusion,  and  its  functions 
may  thus  be  seriously  compromised:  a  result  which  is  more 
likely  to  follow  if  physical  exertion  has  been  undertaken  before 
the  inflammation  has  completely  resolved.  Dilatation  of  the 
heart  may  thus  arise  and  persist;  and  if  the  sac,  when  dis- 
tended, contracts  adhesions  to  the  neighbouring  viscera,  and  is 
unable  to  return  to  its  former  dimensions  when  the  inflamma- 
tion has  subsided,  the  results  will  be  still  more  serious. 

In  this  latter  group  of  cases  with  inflammatory  adhesions 
outside  and  within  the  pericardial  sac,  a  characteristic  syndrome 
{Pick^s  or  Concato^s  disease,  polyorrhomenitis,  polyserositis)  is 
not  uncommon.  The  majority  of  these  patients  suffer  from 
ascites  and  enlargement  of  the  liver  with,  in  addition,  evidences 
of  cardiac  failure  and  sometimes  effusions  into  the  pleural 
cavities  as  well ;  jaundice  may  occur,  but  is  rare.  The  abdominal 
symptoms  are  probably  due  to  chronic  peritonitis,  which  is 
most  marked  upon  the  diaphragmatic  surface  of  the  liver, 
accompanied  by  a  varying  degree  of  hepatic  cirrhosis  ;  but  the 
latter  may  be,  as  in  one  of  Harris's  cases,  wholly  absent  even 


406  DISEASES  OF  THE  HEART 

when  ascites  is  a  prominent  symptom.  In  some  cases  the 
earliest  symptoms  are  cardiac  (as  in  Case  1),  and  the  in- 
flammation originates  within  the  pericardium;  but  in  others 
the  primary  lesion  may  be  pleural,  or  both  the  pleural  and 
pericardial  lesions  may  occur  simultaneously.  The  combina- 
tion is  by  no  means  unusual,  and  occurred  in  3  of  my  cases  of 
acute  pericarditis ;  while  in  6  more  pleurisy  developed  either 
before  or  after  the  pericarditis. 

In  my  series  of  22  cases,  a  diagnosis  of  pericardial  adhesion 
was  made  in  6,  3  of  which  are  reported  below.  In  2  the  diag- 
nosis was  based  upon  the  previous  observation  of  the  acute 
stage.  In  the  sixth,  a  patient  who  died  from  cardiac  failure, 
the  evidences  of  congestion  in  the  area  of  the  superior  vena  cava 
were  persistent  and  in  excess  of  those  in  the  area  of  the  inferior 
cava.  The  pericardial  and  the  right  pleural  sacs  were  obliterated 
b}'  adhesions,  which  in  some  parts  were  ver}-  thick,  the  medias- 
tinum showed  evidences  of  chronic  inflammation,  and  the 
superior  cava  was  narrowed  to  nearly  half  its  diameter  imme- 
diately above  the  right  auricle. 

The  Physical  Signs  of  Adherent  Pericardium.  —  In  many 
cases  no  evidence  of  pericardial  adhesions  is  apparent,  and  the 
diagnosis  is  made  on  yost-ynortem  examination.  This  is  most 
frequently  the  case  when  valvular  disease  co-exists,  as  the 
symptoms  are  naturally  ascribed  to  the  valvular  defect.  A 
knowledge  of  the  previous  occurrence  of  acute  pericarditis 
maj'  suggest  the  existence  of  adhesions,  but  it  must  be  remem- 
bered that  the  signs  of  "adherent  pericardium"  are  really 
those  of  chronic  mediastino-pericarditis,  and  do  not  follow 
mere  adhesion  of  the  visceral  and  parietal  layers. 

In  a  general  way  the  apex  impulse  is  diffuse  and  forcible  and 
displaced;  pulsation  is  also  evident  in  the  epigastrium,  and 
to  the  left  and  often  to  the  right  of  the  sternum ;  the  latter  as 
well  as  the  ribs  may  pulsate  visibty.  In  children  the  prsecordia 
maj^  be  prominent.  The  apex  impulse  may  be  flxed  to  the 
chest  wall  and  show  little  or  no  alteration  in  site,  when  the 
patient  turns  on  to  his  left  side ;  or  in  force,  during  full  inspira- 
tion, if  the  pleural  cavity  is  also  obliterated ;  but  these  signs  are 
really  evidence  of  pleural,  and  not  of  cardiac,  adhesion,  and 
nave  been  found  to  be  present  in  cases  where  the  pericardium 


ADHERENT  PERICARDIUM  407 

was  quite  normal.  Immobility  of  the  lateral  borders  of  cardiac 
dulness,  especially  on  the  left  side,  during  the  respiratory  move- 
ments, owns  a  similar  origin,  and  though  generally  associated 
with  pericardial  adhesions,  may  also  be  a  fallacious  guide. 

The  normal  systolic  protrusion  of  the  apex  impulse  may  be 
replaced  by  systohc  recession  (Fig.  190).  The  explanation  is 
somewhat  difficult  to  understand,  for  the  true  apex  impulse 
must  protrude  during  systole,  as  the  longitudinal  axis  of  the 
heart  is  always  lengthened.  It  seems  probable  that  systolic 
retraction  of  an  interspace  in  the  region  of  the  apex  is  due  to 
right-sided  hypertrophy  with  displacement  of  the  apex  back- 
wards, and  to  the  retraction  of  the  right  ventricle  becoming 
perceptible,  owing  to  its  adhesion  to  the  chest  wall.  A  similar 
recession  of  the  interspaces  close  to  the  sternum  is  often  seen 

■BrokeK 


5  -  Ltf t  Sf>a.c-e. 

Griil.es  ■  "■ 

Fig.  190. — Curves  tkom  the  Brachial  Artery  and  Apex  Impulse,  showing 
Systolic  Retractioist  op  the  Impuxse. 

in  persons  with  hypertrophied  hearts,  as  the  transverse  diameter 
towards  the  base  of  the  ventricle  is  always  shortened  during 
systole,  and  the  atmospheric  pressure  upon  the  surface  of  the 
chest  causes  a  recession.  The  sternum,  too,  may  be  retracted 
during  systole  (Fig.  194);  this  is  probably  always  a  sign  of 
adhesion. 

A  similar  systolic  recession  may  be  found  to  the  right  of  the 
sternum  in  the  fourth  and  fifth  interspaces  from  similar  causes, 
and  even  the  cartilages  may  be  retracted  if  they  are  soft ;  but 
here,  too,  a  fallacy  obtains,  and  Fig.  192  was  taken  from  a 
patient  with  mitral  stenosis,  in  whom  i)ost-7nortem  examination 
showed  neither  pericarditis  nor  meliastinitis,  so  that  the  sign 
is  obviously  inaccurate.  Broadbent  has  described  "  visible 
pulsation,  synchronous  with  the  cardiac  systole,  of  the  left 
back  in  the  region  of  the  eleventh  and  twelfth  ribs,  and  in  less 
degree  of  the  same  region  on  the  right  side,"  as  strongly  sug- 


408  DISEASES  OF  THE  HEART 

gestive  of  the  adhesion  of  the  heart  to  the  diaphragm,  the 
cardiac  contractions  pulHng  the  diaphragm  upwards  and  so 
drawing  the  false  ribs  inwards  with  each  systole;  a  similar 
pulsation  may  be  apparent  on  the  front  of  the  chest  at  the 
anterior  ends  of  the  sixth  and  seventh  ribs.  But  he  has  sub- 
sequently found  the  sign  to  be  present  in  cases  of  hypertrophied 


Fig.  191. — Curves  from  the  Left  Back  Immediately  Below  the  Costal 
Maegin,  and  Just  Outside  the  Line  of  the  Scapular  Angle,  and  the 
Radial  Artery,  showing  that  the  Retraction  in  the  Former  Situation 
IS  Systolic  in  Rhythm  (Broadbent's  Sign). 

heart  without  adhesion,  and  the  pericardium  was  normal  in 
the  onty  case  in  which  I  have  observed  it  (Fig.  192). 

Adhesion  of  the  heart  to  the  diaphragm  or  to  the  sternum 
may  prevent  or  limit  their  movements  during  respiration. 
The  defect  in  abdominal  movement  is  read^'ly  appreciated  by 
the  eye  or  by  the  hand.  Deficiency  in  the  respiratory  move- 
ment of  the  sternum  is  best  shown  with  the  cahpers,  for  the 
increase  in  the  antero-posterior  diameter  of  the  chest  is  slight, 


Fig.  192. — Curves  from  the  Fourth  Right  Interspace  and  Apex  Impulse, 
SHOWING  Systolic  Retraction  of  the  Former. 

rarely  exceeding    1  inch  in  normal  individuals,  and  is  always 
limited  in  emphysema  and  in  pigeon-breast. 

The  pulse  is  generally  rather  small  and  somewhat  frequent 
in  cases  which  come  under  observation  on  account  of  cardiac 
insufficiency.  It  frequently  varies  both  in  volume  and  force 
with  the  respirator}'  movements,  becoming  larger  and  stronger 
during  expiration  {pulsus  paradoxus,  Fig.  193),  the  exact  oppo- 
site of  the  normal,  but  this  has  been  observed  in  pericardial 


ADHERENT  PERICARDIUM 


409 


effusion,  and  even  in  cases  where  the  heart  was  normal.  Faihire 
of  the  pulse  during  full  inspiration,  however,  does  not  seem  to 
occur  unless  mediastino-pericarditis  is  present.  Pulsus  para- 
doxus is  probably  due  in  these  cases  to  adhesions  about  the 
root  of  the  heart,  embracing  the  aorta  and  the  great  veins ;  and 
to  traction  exerted  upon  the  fibrous  bands  during  inspiration 
narrowing  their  lumen  and  so  limiting  both  the  output  and  the 
intake  of  the  heart.  Inspiratory  filhng  of  the  cervical  veins 
(Kiissmaul's  sign)  owns  a  like  cause,  and  may  also  be  present. 

The  pulse  may  of  course  present  the  characteristic  features 
of  that  of  aortic  regurgitation  or  renal  cirrhosis,  should  either 
of  these  conditions  co-exist. 

The  other  signs  which  have  been  described  are  less  frequently 
present,  and  may  be  due  to  many  causes.     Sir  W.  Broadbent 


Fig.  193. 


-Ctteves  of  Respieatoey  Movements  and  Radial  Pulse:  Pulsus 
Paeadoxus. 


The  pulse  is  largest  during  expiration. 


drew  attention  to  the  fact  that  the  diastolic  shock  of  the  arterial 
valvular  closure  was  often  well  marked  and  felt  over  a  large 
area ;  but  this  may  also  obtain  in  dilatation  of  the  aorta  and  in 
high  blood-pressure.  Riess  has  described  cases  in  which  the 
cardiac  sounds  were  of  metallic  quality  and  well  conducted 
to  the  skin  surface  overlying  the  stomach.  Sewill  has  reported 
reduplication  of  the  first  sound ;  and  Thayer  thinks  that  the 
third  cardiac  sound  is  usually  very  distinct.  All  these  signs, 
however,  are  infrequent  in  adherent  pericardium,  and  may 
be  present  in  other  cardiac  abnormahties . 

None  of  the  signs  ascribed  to  pericardial  adhesions  are  thus 
pathognomonic,  and  they  may  all  be  absent  in  individual 
cases. 

A  patient  died  recently  in  my  wards  from  valvular  disease 
of  the  heart  who  had  previously  suffered  from  an  attack  of  acute 
pericarditis  of  rheumatic  origin  under  my  observation.    A  week 


410  DISEASES  OF  THE  HEART 

before  her  death  I  carefully  examined  her  for  all  the  signs  of 
adherent  pericardium  which  have  been  described  above,  with 
the  exception  of  Reiss's  sign  and  immobility  of  the  apex  impulse 
on  change  of  position.  All  were  absent,  but  post-mortem  ex- 
amination showed  that  the  pericardial  sac  was  entirely  obliter- 
ated by  fairly  firm  adhesions.  The  heart,  however,  was  not 
adherent  to  the  chest  wall,  mediastinitis  was  minimal  and  in  no 
way  indurative,  and  the  pleural  cavities  were  normal. 

The  previous  existence  of  pericarditis  ;  the  presence  of  several 
signs  in  conjunction,  in  particular  a  well-marked  systolic  re- 
traction of  a  powerful  apex  impulse  or  of  the  sternum ;  immo- 
bihty  of  the  impulse  and  the  borders  of  cardiac  dulness  during 
respiration ;  and  the  occurrence  of  cardiac  insufficiencj^  without 
any  other  obvious  cause,  are  strongly  in  favour  of  the  presence 
of  mediastino-pericarditis.  Examination  with  the  Rontgen 
raj-s  is  often  valuable.  The  mediastinal  induration  may  be 
apparent  in  skiagrams  (Fig.  195),  and  limitation  of  the  move- 
ment of  the  diaphragm  from  the  presence  of  adhesions  may  be 
visible  with  the  screen. 

The  following  cases  illustrate  the  usual  symptoms  of  Pick's 
disease : 

Case  1. — A  boy,  aged  sixteen,  was  admitted  into  hospital 
on  May  11,  1908,  complaining  of  breathlessness  and  of  pain  in 
the  left  side  of  the  chest,  and  of  swelling  of  the  abdomen  and 
of  the  face  and  feet. 

He  had  always  been  healthy,  save  for  an  attack  of  scarlatina 
in  childhood,  until  he  contracted  rheumatic  fever  four  months 
before  admission.  Many  joints  were  affected,  and  he  sweated 
profusely,  and  was  confined  to  bed  for  three  weeks.  Even 
when  he  was  lying  in  bed  he  was  very  breathless,  and  this 
continued  for  a  month  after  he  got  up,  being  intensified  on 
exertion,  and  he  spent  the  greater  part  of  this  time  in  bed. 
The  dyspnoea  then  lessened,  but  he  was  still  unfit  to  return  to 
his  work  at  the  pit.  Three  weeks  before  admission,  the  lower 
eyelids  and  the  feet  became  swollen,  and  the  abdomen  was 
noticed  to  be  enlarging,  and  he  was  again  forced  to  return  to 
bed.  He  had  a  slight  cough  without  any  spit,  and  his  left 
side  became  painful  at  times,  but  otherwise  he  had  no  special 
discomfort  J  and  his  appetite  was  good. 


ADHERENT  PERICARDIUM  411 

On  admission,  he  was  found  to  be  a  well -grown  lad  of  fair 
nutrition.     He  lay  flat  in  bed,  by  preference  on  his  right  side. 

There  was  slight  oedema  in  the  legs  and  over  the  sacrum, 
but  none  in  the  face,  and  his  complexion  was  somewhat  pale. 
The  tongue  was  coated  and  rather  dry,  and  the  pharynx  was 
congested.  The  abdomen  was  considerably  distended  and 
contained  a  large  quantitj^  of  free  fluid.  The  spleen  could 
not  be  felt,  but  the  hver  was  definitely  enlarged.  Rhonchi 
were  audible  aU  over  the  chest  and  rales  at  the  posterior 
bases . 

His  progress  thereafter  was  satisfactory.  The  <Dedema  and 
ascites  rapidly  disappeared,  and  he  left  hospital  on  September 
12,  1908,  in  fair  health,  and  resumed  his  work  as  a  colher.  He 
continued  at  work  until  March,  1909,  when  the  abdomen  again 
began  to  swell,  and  as  he  became  unable  to  stoop  he  had  to 
cease  work.  There  was  no  recurrence  of  the  general  oedema, 
and  no  other  symptoms  beyond  shght  breathless ness  on  exer- 
tion ;  but  the  ascites  increased,  and  he  was  again  forced  to  go 
to  bed  in  July. 

On  admission  in  August,  he  seemed  to  have  lost  flesh,  and 
he  was  pale  and  thin.  He  lay  easily  in  bed  and  made  no 
complaint,  though  the  ascites  was  now  much  greater  than  on 
his  first  admission,  but  there  was  no  oedema.  His  progress, 
however,  was  not  satisfactory.  The  ascitic  accumulation  had 
to  be  removed  frequently,  as  it  rapidly  recurred  after  tapping. 
The  fiuid  presented  the  characters  of  a  transudate,  the  cellular 
elements  being  mainty  lymphocytes,  with  some  large  endo- 
thelial cells,  which  were  often  en  jilaque,  and  a  few  polymorpho- 
nucleated  cells.  In  December  he  was  transferred  to  a  surgical 
ward  for  operation.  Death  ensued  suddenty,  when  he  was 
under  the  anaesthetic,  before  any  operative  interference  had 
been  undertaken. 

The  physical  signs  which  were  observed  during  life  were  not 
very  distinctive  evidence  of  adherent  pericarditis.  There  was 
no  pulsation  on  the  front  of  the  chest,  though  the  apex  impulse 
could  be  felt  indistinct^  in  the  fifth  left  space  when  he  lay  on 
his  left  side.  The  area  of  cardiac  duhiess  was  of  normal  site 
and  size,  but  was  not  altered  by  changes  in  position  or  in  re- 
spiration.    The  cardiac  sounds  were  pure  but  short.     On  his 


412  DISEASES  OF  THE  HEART 

first  admission,  murmurs  were  present  from  time  to  time,  both 
at  the  apex  and  at  the  base,  but  they  never  persisted  for  any 
length  of  time;  on  his  second  admission  the  sounds  were  pure. 
The  pulse  was  always  quite  regular,  but  a  Httle  frequent  (90  to 
100).  The  chest  expansion  measured  2  inches,  and  the  dia- 
phragm moved  fairly  well  with  respiration.  There  was  no 
inspiratory  distension  of  the  cervical  veins,  though  there  was 
a  shght  pulsus  paradoxus,  and  there  was  no  systolic  drag  upon 
the  false  ribs ;  but  the  liver  was  large,  and  steadily  increased 
in  size  (the  vertical  measurement  being  7|  inches  on  his  second 
admission),  and  the  ascitic  transudation  with  minimal  oedema 
pointed  to  a  hepatic  origin.  The  antecedent  rheumatism 
accompanied  by  breathlessness  while  at  rest  suggested,  in  the 
absence  of  gross  pulmonary  lesions,  a  cardiac  origin,  and  a 
diagnosis  of  adherent  pericardium  and  perihepatitis  was 
accordingly  made. 

On  post-mortem  examination,  the  pleural  cavities  were  found 
to  be  completely  abolished  by  firm  adhesions  everywhere,  save 
at  the  base  of  the  right  lung,  where  2  pints  of  fluid  were  present 
between  the  diaphragm  and  the  base  of  the  lung.  The  peri- 
cardial surfaces  were  united  by  firm  adhesions,  which  were 
fully  half  an  inch  thick  in  places,  and  the  diaphragm  was 
firmly  adherent  to  both  liver  and  spleen,  the  hepatic  peritoneum 
elsewhere  being  only  slightly  thickened.  The  liver  was  con- 
siderably enlarged  and  showed  an  early  fine,  monolobular 
cirrhosis.     The  cardiac  valves  were  normal. 

Case  2. — ^A  pithead  w^orker,  aged  seventeen,  was  achnitted 
to  hospital  on  June  10,  1911,  complaining  of  swelling  of  the 
feet  and  legs  of  five  months'  duration. 

His  previous  health  had  not  been  good.  He  had  had 
whooping-cough  and  measles  in  childhood,  and  had  fallen  and 
broken  two  of  the  right  ribs  at  the  age  of  thirteen,  and  shortly 
afterwards  was  admitted  into  hospital  on  account  of  ascites 
with  occasional  attacks  of  pain  in  the  right  iliac  fossa.  In 
July,  1907,  the  abdomen  w^as  opened,  and  the  intestines  were 
found  to  be  covered  with  miliary  tubercles.  He  made  a  good 
recovery,  and  worked  for  eight  months  at  the  pithead,  but 
the  ascites  recurred,  and  in  July,  1908,  as  the  scar  of  the 
former  wound  was  thin  and  distended,  the  abdomen  was  again 


ADHERENT  PERICARDIUM  413 

opened.  The  liver  was  now  enlarged  and  rough,  so  an  attempt 
was  made  to  procure  adhesions  between  it  and  the  parietal 
peritoneum.  On  dismissal  in  September,  his  general  condition 
had  improved,  but  he  was  distinctly  cyanosed  and  had  a 
troublesome  cough.  He  was  unable  to  return  to  work  as  the 
cough  continued,  accompanied  by  a  yellow  spit,  and  he 
was  breathless,  and  felt  his  heart  beating  on  any  exertion, 
and  oedema  appeared  at  times  in  the  feet  and  legs.  In 
January,  1911,  the  oedema  became  permanent  and  gradually 
increased  in  extent,  and  the  breathlessness  became  more 
marked. 

On  admission,  the  patient  lay  comfortably  flat  in  bed.  He 
was  only  moderately  developed,  and  was  poorh^  nourished, 
and  there  was  widespread  oedema,  though  it  was  not  extreme. 
The  mucous  membranes  were  very  blue,  and  the  face  was  puffy, 
and  the  hands  and  feet  were  congested  and  purple.  The  malar 
capillaries  were  distended  and  prominent.  The  tongue  was 
moist  and  coated.  The  abdomen  was  large  but  not  tender. 
The  parietes  were  oedematous.  and  there  was  shght  ascites. 
The  hver  was  enlarged,  but  not  tender,  the  vertical  measure- 
ment being  6|-  inches,  the  edge  and  surface  being  smooth  and 
firm;  it  moved  Yevj  slightly  with  respiration,  the  movement 
on  the  left  side  being  more  ample,  though  distinctty  less  than 
normal.  The  spleen  was  slighth'  enlarged.  The  respiratory 
murmur  over  the  right  lower  back  and  axilla  was  deficient  and 
accompanied  by  much  fine,  bubbling  rale. 

The  patient  remained  in  hospital  until  November,  but  re- 
ceived shght  benefit  from  his  treatment.  He  made  httle  com- 
plaint, and  had  few  discomforts  when  he  was  confined  to  bed, 
but  the  oedema  increased  whenever  he  was  out  of  bed  for 
any  length  of  time. 

There  was  well  -  marked  pulsation  over  the  front  of  the 
chest,  the  whole  prsecordia  heaving,  though  it  was  not  unduly 
prominent.  The  apex  impulse  was  fixed  and  was  unaltered 
by  changes  in  position  or  by  the  respiratory  movements,  and 
was  negative,  a  sj^stolic  retraction ;  and  the  third,  fourth, 
fifth,  sixth,  and  seventh  cartilages  on  both  sides,  but  less 
strongly  on  the  right,  and  the  lower  sternum  (Fig.  194)  showed 
similar  movements,  the  interspaces  moving  more  freely  than 


414  DISEASES  OF  THE  HEART 

the  cartilages.  The  sternal  pulsation  was  exaggerated  on  deep 
inspiration.  The  area  of  dulness  was  enlarged  on  both  sides, 
and  was  not  influenced  by  the  respiratory  movements.  The 
cardiac  sounds  were  pure,  the  first  sound  being  everywhere 
short  and  sharp  and  loud.  The  pulse  was  always  regular,  but 
a  little  frequent  (90  to  100).  The  blood-pressure  was  normal. 
There  was  distinct  pulsus  paradoxus,  and  the  sternal  move- 
ment forwards  on  inspiration  was  nil.  Broadbent's  sign  was 
absent,  and  there  was  no  visible  distension  of  the  cervical 
veins  at  any  time. 

A  skiagram  showed  considerable  mottling  on  each  side  of 
the  heart,  especially  to  the  right.  The  right  heart  was  en- 
larged, and  the  cardio-hepatic  angle  was  obtuse,  and  the  upper 
margin  of  the  diaphragm  was  indistinct. 


X  nSjbt/1. 


■*** 


=  TolA.£     reA^K 


<-*^^      ^       S    h.«^VVK    . 


Fig.  194. — Curves  of  Respiratory  Movements   and  Retraction  of  Lower 

End  of  Sternum. 

The  history  of  this  case  presents  an  absence  of  the  usual 
causes  of  mediastino-pericarclitis,  and  the  injury  to  the  ribs 
which  preceded  the  onset  of  the  ascites  was  the  only  illness 
known  which  niight  affect  the  thoracic  viscera.  The  presence 
of  diffuse  tuberculosis  in  the  abdomen  at  the  time  of  the  first 
operation,  however,  suggests  another  cause,  chronic  tuber- 
culosis in  the  mediastinum ;  and  the  localization  of  rale  to  the 
right  lower  lobe  alone  and  the  diminution  of  the  respiratory 
murmur  pointed  to  a  local  pulmonary  lesion,  although  no  de- 
finite signs  of  a  massive  consolidation  were  present.  No  tubercle 
bacilli  could  be  found  in  the  sputum.  There  is  in  the  Museum 
of  the  Western  Infirmary  a  specimen  of  a  heart  with  an  enorm- 
ously thickened  (tubercular)  pericarditis,  which  arose  from 
the  direct  infection  of  the  pericardium  by  a  tubercular  gland 
in  the  mediastinum.  The  whole  of  the  mediastinum  was 
matted  together  around  caseous  glands,  and  a  tuberculous 
pleurisy  co-existed,  so  that  the  factors  required  for  further 


ADHERENT  PERICARDIUM  415 

spread  were  already  present.  In  Harris's  series  of  25  cases  11 
seemed  to  be  due  to  tuberculosis. 

Case  3. — A  cabinet-maker,  aged  twenty-seven,  was  ad- 
mitted to  hospital  on  July  1,  1909,  on  account  of  a  right 
hemiplegia  which  had  occurred  suddenly  two  days  previously. 

His  health  had  been  good  until  two  years  before  admission, 
when  he  became  subject  to  "  indigestion,"  which  was  occasion- 
ally accompanied  by  vomiting.  His  face  was  at  times  swollen, 
and  he  was  short  of  breath,  and  for  the  last  six  months  had 
been  troubled  with  headache  and  swelling  of  the  abdomen. 
Two  months'  before  admission  he  had  to  cease  work  for  a 
fortnight  on  account  of  abdominal  pain  and  swelling  accom- 
panied by  headache  and  vomiting. 

He  was  an  unhealthy-looking  man,  of  poor  physique.  The 
face  was  puffy  and  covered  with  acne,  and  the  venules  on  the 
nose  were  dilated.  The  eyeballs  were  rather  prominent,  and 
there  were  slight  nystagmoid  movements  when  the  eyes  were 
turned  to  the  side.  The  veins  on  the  forehead  were  dilated 
and  prominent,  and  the  left  jugular  veins  were  large  and  full. 
The  muscles  were  small  and  soft,  and  enlarged  glands  were 
present  in  the  axillae  and  groins.  The  tongue  was  coated, 
many  of  the  teeth  were  carious,  and  the  tonsils  were  enlarged 
and  inflamed.  The  abdomen  was  large,  mainly  on  account  of 
enlargement  of  the  liver,  which  occupied  the  greater  part  of 
the  right  hypochondrium ;  the  area  of  dulness  measured 
7^  inches  vertically.  The  edge  was  thickened  and  hard, 
and  not  tender,  and  moved  but  little  with  respiration.  A 
small  amount  of  free  fluid  was  present  in  the  abdomen.  Im- 
provement was  rapid,  and  power  steadily  returned  to  the 
paralyzed  limbs,  while  his  speech  regained  clearness  and 
accuracy. 

In  the  middle  of  July  he  suddenly  experienced  acute  pain 
in  the  right  hypochondrium,  and  the  pulse  became  more  fre- 
quent. The  liver  was  distinctly  larger  than  it  had  been,  and 
was  now  tender  to  palpation,  and  friction  was  audible  over 
the  lower  part  of  the  right  chest.  The  symptoms  subsided 
within  ten  days,  and  the  hepatic  tenderness  disappeared  and 
the  liver  returned  to  its  usual  dimensions.  Improvement 
continued,  and  he  was  able  to  go  home  on  September   13. 


416  DISEASES  OF  THE  HEART 

walking  fairly  well.  His  colour,  however,  had  deepened,  and 
he  was  more  cyanotic  than  on  admission. 

He  was  readmitted  to  hospital  on  March  31,  1910,  on  ac- 
count of  pain  and  swelling  in  the  abdomen  and  oedema  in  the 
legs.  The  pain  had  recurred  on  five  occasions  in  the  interval. 
It  was  never  very  severe,  but,  commencing  gradually,  steadily 
increased  for  a  week  or  so,  and  then  gradually  disappeared 
after  ten  days  or  a  fortnight.  The  bowels  were  costive  during 
the  attacks,  but  there  was  no  vomiting.  The  symptoms  had  been 
more  severe  since  January,  and  the  legs  had  become  swollen. 

On  admission,  he  was  more  cyanotic  than  before,  and  he 
required  three  pillows  on  his  bed.  There  was  severe  ascites, 
and  oedema  in  the  limb  which  had  been  paralyzed  though  there 
was  none  in  the  other,  and  he  was  short  of  breath  and  incap- 
able of  any  exertion. 

The  prsecordium  generally  was  prominent,  and  there  was  well- 
marked  pulsation  in  the  second,  third,  fourth,  fifth,  and  sixth 
left  interspaces,  the  maximum  being  in  the  fifth  and  negative, 
a  retraction  during  systole  (Fig.  190) ;  and  with  diastole  a  well- 
marked  shock  was  felt  on  palpation  all  over  the  right  chest. 
The  impulse  moved  for  nearly  an  inch  when  he  turned  on  to 
his  left  side,  and  decreased  in  force  during  inspiration.  The 
area  of  dulness  was  of  normal  site  and  size,  but  the  right  border 
was  unaffected  by  respiration.  There  was  pulsation  in  the 
epigastrium,  which  was  S3'stolic  in  rhythm.  All  the  veins  of 
the  body  were  prominent  and  full,  and  the  valves  stood  out  dis- 
tinctly, the  veins  on  the  sides  of  the  chest  and  the  left  external 
jugular  being  most  distinct ;  one  on  the  left  flank  was  varicose. 
On  auscultation,  the  sounds  were  everywhere  pure,  but  every- 
where triple.  The  first  sound  was  somewhat  loud,  but  short 
and  sharp,  and  the  emphasis  was  on  the  middle  sound.  The 
pulse  was  small  and  poorly  sustained,  and  about  the  normal 
rate.  During  his  first  residence  it  was  quite  regular,  save  for 
occasional  extra-systoles,  but  during  his  second  stay  it  waS' 
always  irregular  (auricular  fibrillation).  A  skiagram  showed 
considerable  fibrosis  of  the  right  lung,  which  was  most  marked 
at  the  base,  where  it  was  intimately  mingled  with  the  shadow 
of  the  diaphragm  and  the  right  border  of  the  heart  (Fig.  195), 
The  lower  interspaces  of  the  chest  were  retracted  on  inspiration. 


ADHERENT  PERICARDIUM  417 

The  false  ribs  showed  no  cardiac  movement,     SHght  pulsus 
paradoxus  was  present. 

The  diagnosis  in  this  case  seemed  clear,  but  the  cause  was 
not  very  apparent  at  first.     On  examination,  however,  a  scar 


Fio.   195. — Skiagram  from  a  Case  of  Mediastixo-Pericarditis,  associated 
WITH  Chronic  Pleueo-Pneumonia  of  Right  Lung  (J.  R.  R.). 

was  found  at  the  lower  part  of  the  right  chest  behind  where 
an  "  abscess  "  had  been  opened  in  childhood,  and  there  was 
dulness  and  deficient  respiratory  murmur  in  this  situation,  so 
that  it  seemed  probable  that  an  empyema  had  been  present. 

27 


418  DISEASES  OF  THE  HEART 

The  recurring  attacks  of  perihepatitis,  however,  suggested  the 
existence  of  an  active  focus  of  infection,  but  none  could  be 
discovered  beyond  the  tonsillar  inflammation  and  a  slight 
catarrh  in  the  lungs. 

REFERENCES. 
Sm  John  Broadbent:  Adlierent  Pericardium,     London.     1895. 
Thomas  Harris :  Indurative  Mediastino -Pericarditis.    London.    1895. 
Pick:  Zeitschr.  f.  klin.  Med.,  1895,  vol.  xxix.,  p.  385. 
A.  O,  J.  Kelly:    Amer.  Journ.  Med.  Sci.,  1903,  vol.  cxxv.,  p.  116. 

Pneumo  -  Pericardium.  —  The  presence  of  gas  within  the 
pericardial  sac  is  extremely  rare,  James,  when  recording  his 
own  case  in  1904,  being  only  able  to  find  37  undoubted 
cases  in  the  literature.  To  these  I  can  but  add  the  case 
recorded  by  Ljungdahl  in  1913,  and  that  which  is  reported 
below, 

Pneumo-pericardium  may  conceivably  arise  in  several  ways. 
In  a  few  cases  it  has  apparently  developed  post-mortem  from 
infection  of  the  sac  by  a  gas-producing  organism ;  but  no  case 
has  yet  been  recorded  in  which  such  an  occurrence  has  been 
observed  during  life,  and  in  only  5  of  James's  cases  was  the 
pericardium  closed,  though  in  Ljungdahl's  and  in  my  own  case 
no  evidence  of  a  breach  of  continuity  was  discovered. 

In  a  second  group  the  gas  is  due  to  the  entrance  of  air 
through  a  wound.  This  has  occurred  in  compound  fractures  of 
the  thorax,  stabs,  gunshot  wounds,  and  operative  procedures 
such  as  paracentesis  of  the  pleural  cavity,  and  has  been  pro- 
duced as  a  therapeutic  measure  by  Wenckebach  in  chronic 
pericardial  effusion,  apparently  with  benefit. 

In  a  third  group  pneumo-pericardium  is  due  to  ulcerative 
processes  connecting  the  sac  with  an  air-containing  viscus. 
The  primary  lesions  have  been  varied — ulcerating  cavities  in 
the  lung,  both  tubercular  and  gangrenous ;  pyo-pneumo- 
thorax ;  oesophageal  ulceration,  both  cancerous  and  traumatic  ; 
and  subdiaphragmatic  abscess  due  to  gastric  ulcer,  hepatic 
abscess,  and  even  appendicitis. 

In  the  majority  of  cases  the  lesion  which  permits  the  pneumo- 
pericardium produces  in  addition  an  infection  of  the  sac,  and 
effusion  sooner  or  later  develops,  and  very  often  becomes 
purulent.     The  symptoms  and  the  physical  signs  are,  in  conse- 


ADHERENT  PERICARDIUM  419 

quence,  as  a  rule  due  in  part  to  pericarditis,  and  in  part  to  the 
aerial  distension  of  the  sac. 

The  onset  of  the  symptoms  may  be  gradual  or  sudden.  In 
the  former  case  the  symptoms  are  those  of  acute  pericarditis ; 
in  the  latter  the  sudden  occurrence  of  cyanosis,  collapse,  syn- 
cope, prsecordial  oppression,  or  pain,  denotes  the  advent  of  the 
new  lesion. 

The  physical  signs  are  usually  striking.  The  apex  impulse 
disappears,  though  it  has  been  noticed  to  return  if  the  patient 
assumed  the  prone  position,  and  the  area  of  cardiac  dulness  is 
replaced  by  an  area  with  a  tympanitic  or  skodaic  note.  In 
Stokes's  case  a  b7'uit  de  pot  fele  was  present  for  a  time.  As 
effusion  develops,  the  area  of  tympanitic  percussion  sound 
becomes  diminished  and  varies  in  site  according  to  the  position 
of  the  patient.  The  auscultatory  phenomena  at  this  stage  are 
characteristic,  and  the  cardiac  contractions  produce  the 
rhythmic  churning,  splashing,  "  miU- wheel  "  sounds,  which 
are  distinctive  of  the  presence  of  air  and  fluid  within  the  peri- 
cardium. In  Stokes's  case  they  had  a  peculiar  metallic 
character;  metallic  tinkhng  has  frequently  been  noticed. 
Friction  sounds  of  the  usual  kind  often  co-exist. 

In  the  majority  of  cases  the  diagnosis  has  been  eas}",  as  only 
6  of  James's  cases  were  not  recognized  before  autopsy.  In 
my  case,  however,  the  condition  was  only  diagnosed  on 
examination  with  the  X  raj'S,  but  in  this  instance  the  charac- 
teristic auscultatory  and  percussion  phenomena  were  absent, 
as  effusion  did  not  develop,  and  the  heart  maintained  through- 
out its  normal  relation  to  the  front  of  the  chest.  The  disten- 
sion of  the  sac,  too,  at  the  first  X-ray  examination  was  slight. 
The  diagnosis  in  Ljungdahl's  case  was  also  made  with  the 
X  rays,  but  no  photograph  was  taken. 

The  prognosis  in  pneumo-pericardium  is  better  than  might 
be  anticipated,  for  11  of  James's  cases  recovered,  so  that  13 
out  of  40  cases  did  not  die.  In  many  of  the  fatal  cases,  too, 
the  primary  lesion  was  evidently  likely  to  prove  fatal. 

The  treatynent  of  this  disease  must  be  conducted  on  orclinar}^ 
lines.  Pyo-pneumo-pericardium  suggests  the  advisabihty  of 
surgical  interference  if  the  general  condition  of  the  patient 
permits. 


420  DISEASES  OF  THE  HEART 

I  have  onl}'  seen  one  case  of  pneumo-pericardium,  and  the 
physical  signs  were  somewhat  different  to  those  which  have 
been  reported.  The  skiagrams,  however,  made  the  diagnosis 
clear. 

A  boy,  aged  eight,  was  admitted  into  hospital  on  October  2, 
1912,  on  account  of  sickness  and  vomiting  of  four  days' 
duration. 

He  had  always  been  healthy  until  his  present  illness,  save 
for  an  attack  of  measles  in  infanc}',  and  had  seemed  in  good 
health  on  September  28.  Next  morning  he  felt  sick  and 
vomited,  and  his  mother  kept  him  in  bed.  The  vomiting  re- 
curred, and  he  became  fevered,  and  was  restless  and  rambled 
in  his  talk.  The  symptoms  persisted,  and  on  October  1  he 
complained  of  headache,  and  frequently  put  his  hands  up  to 
his  occiput. 

On  admission,  he  was  mildly  delirious  and  very  restless,  and 
constantly  moved  his  limbs  in  an  erratic  wa}'.  He  often  placed 
his  hands  at  the  back  of  his  head.  The  skin  was  pale,  dry,  and 
harsh.  The  face  was  flushed  and  the  conjunctivae  were  in- 
flamed. He  took  his  drinks  well,  but  passed  both  urine  and 
faeces  in  bed.  There  were  few  objective  signs.  There  was  a 
slight  catarrh  in  the  chest,  and  the  tongue  was  dry  and  brown. 
The  left  membrana  tympani  showed  some  old  cicatrices,  and 
the  right  a  large  chronic  perforation,  from  which  issued  a  very 
small  quantity  of  slightly  odorous  muco-pus ;  but  there  was 
no  mastoid  tenderness,  and  no  palsy  or  spasm  or  inequality  of 
reflex  could  be  discovered,  save  that  the  right  pupil  was  slightly 
larger  than  the  left.  Kernig's  sign  was  negative.  During  the 
succeeding  week  slight  improvement  ensued,  the  delirium  be- 
coming less  and  the  pulse-rate  diminishing  in  frequency.  On 
October  5,  however,  the  stools  contained  a  considerable  amount 
of  muco-pus,  which  persisted  for  twelve  days.  The  pupillary 
inequality  was  inconstant.  Rales  were  now  audible  at  the 
bases  of  the  lungs.  On  October  14,  however,  he  suddenly 
became  extremely  livid  and  very  ill,  and  appeared  to  suffer 
abdominal  pain.  On  October  17  the  abdomen  was  for  the 
first  time  somewhat  distended,  and  a  small  consolidation  was 
discovered  at  the  base  of  the  right  lung.  On  the  20th  new- 
physical  signs  were  recognized  on  the  front  of  the  chest.     The 


ADHERENT  PERICARDIUM 


421 


percussion  note  at  the  left  apex  Avas  skodaic  in  character,  and 
an  area  of  dulness  ran  outwards  from  the  heart  to  the  left 
shoulder;  the  respiratory  murmur  was  ver}^  deficient  (Fig.  196). 
The  area  of  cardiac  dulness  was  increased  in  every  direction. 
The  signs  at  the  right  base  were  unaltered.  Little  change  was 
noticed  during  the  next  few  days,  but  the  duU  area  on  the 
front  of  the  chest  had  disappeared  on  the  26th,  t  hough  the 
respiratory  murmur  at  the 
left  apex  was  stiU  very 
deficient. 

His  general  condition 
slowly  improved,  though 
the  cerebral  symptoms 
still  persisted.  On  No- 
vember 12  the  chest  was 
carefully  examined,  and 
the  area  of  tympanitic 
percussion,  shown  in  Fig. 
197,  was  now  recognized. 
It  may  have  been  present 
for  a  few  days  previously, 
as  the  chest  was  not  ex- 
amined on  every  day .  The 
apex  impulse  persisted  in 
the  fifth  interspace  just 
within  the  nipple  line. 
The  consolidation  at  the 
right  base  was  larger  than 
it  had  been.  Progress 
thereafter  was  continuous, 
though  slow .  The  physical 
signs  gradually  cleared  up 
the  chest  seemed  normal. 


20.X.12 

Fig.   196. — Pneumo-Peeicardium. 
Physical  signs  on  October  20, 


and  on  December  6  the  front  of 
The  liver  was  stiU  enlarged  and 
the  basal  consolidation  was  resolving.  On  dismissal,  on 
January  19,  1913,  he  was  fat  and  well,  though  the  pulse-rate 
was  still  rather  frequent.  In  June,  1913,  he  was  very  well 
and  attending  school  regularly.  There  was  still  some  dulness 
and  deficiency  of  the  respiratory  murmur  at  the  right  base. 
During  his  residence  in  hospital  the  fever  was  slight  and 


4:22 


DISEASES  OF  THE  HEART 


only  exceeded  100°  F.  on  October  19,  20,  and  22,  reaching  a 
maximum  of  100-8°  on  the  latter  date.  It  never  rose  above 
99°  after  December  1 6.  The  pulse-rate  rose  to  1 56  on  October  3 
and  afterwards  ran  about  125  until  the  second  week  of  De- 
cember, when  it  tended  to  run  at  lower  levels,  but  it  was  still 
in  the  neighbourhood  of  100  on  dismissal.  The  respirations 
numbered    44  on   October    5,  and   thereafter   ran   about    30, 

falling  to  normal  limits  in 
the  middle  of  December. 

The  case  presented  man}?- 
interesting  features,  and 
an  accurate  diagnosis  of 
the  sequence  of  events  is 
impossible.  On  admission 
it  seemed  probable  that 
he  was  suffering  from 
meningitis,  but  no  source 
of  infection  was  apparent ; 
the  aural  sepsis  seemed 
quiescent,  and  the  course 
of  events  soon  showed  that 
the  disturbance  was 
general.  The  Widal  test, 
etc.,  were  all  negative,  no 
sputum  could  be  obtained, 
and  a  septicaemia  of  un- 
known nature  was  the  only 
diagnosis.  The  cause  of 
the  exacerbation  of  the 
symptoms  on  October  14 
was  not  recognized,  and 
the  pneumonia  was  not  apparent  until  three  days  later. 
The  interpretation  of  the  new  physical  signs  on  October  20 
was  also  difficult,  and  it  was  only  on  October  28  that  his 
general  condition  permitted  examination  by  the  X  rays,  and 
the  pneumo-pericardium  was  recognized.  The  skiagrams  are 
instructive.  On  October  28  the  distension  of  the  pericardium 
was  probably  uniform,  the  heart  was  but  little  displaced,  and 
the  pneumonia  was  small  (Fig.   198).     On  November  11  the 


12.XI.12. 

Fig.  197. — Pnetjmo -Pericardium. 
Physical  signs  on  November  12. 


ADHERENT  PERICARDIUM 


423 


distension  of  the  sac  was  considerably  larger,  but  only  towards 
the  left  side  and  immediately  below  the  apex,  and  the  heart 
was  displaced  towards  the  right.  On  November  22  the  heart 
still  seemed  displaced,  but  the  gas  was  in  less  amount  and  almost 


<J    c 
o 

S     S 


Ph 


«»       CE 


f=H 


wholly  on  the  left  side  (Fig.  199).  On  December  6  the  disten- 
sion was  less  and  the  heart  had  returned  to  its  normal  site. 
On  December  16  the  distension  was  still  less,  and  subsequent 
skiagrams  failed  to  reveal  any  gas  in  the  pericardial  sac.     The 


424 


DISEASES  OF  THE  HEART 


distension  of  tlie  pericardial  sac,  however,  was  never  quite 
uniform,  for  the  apex  impulse  persisted  throughout,  and  the 
area  of  cardiac  dulness  also  remained,  so  that  the  heart  can 
never  have  left  the  front  of  the  chest.  There  was  at  no  time 
any  evidence  of  pericarditis,  and  there  was  no  history  of  any 
illness  in  the  past  likely  to  have  produced  pericardial  adhesion, 
so  that  the  cause  of  the  localization  of  the  gas  is  unknown. 


M^GLONE 


Fig.  199. — Pneumo-Pekicardium  (J.  R.  R.). 
Skiagram  taken  on  November  22. 


It  seems  possible  that  the  original  septicaemia  provoked  (or 
originated  in)  a  local  lesion  of  the  mediastinal  glands,  which  on 
October  14  became  disseminated  more  widely,  involving  first  of 
all  the  right  lung  and  subsequently  the  pericardium,  and  per- 
mitting the  entrance  of  air  into  the  pericardium  from  the  lung. 

Thepossibihty  of  a  gas-producing  infection  of  the  pericardium 
seems  slight,  for  at  no  time  was  pericardial  friction  observed, 
and  the  skiagrams  exclude  the  presence  of  effusion. 


ADHERENT  PERICARDIUM  425 

Tile  only  skiagram  which  I  can  discover  in  the  hterature  is 
that  which  was  taken  in  Wenckebach's  case.  It  differs  in 
some  respects  from  Figs.  198  and  199.  The  heart  appears  to 
be  in  its  usual  situation,  and  is  not  displaced.  The  pericardial 
sac  is  uniformly  distended  and  projects  well  to  the  right  of  the 
right  auricle.  The  upper  margin  (as  in  Fig.  199)  extends  higher 
upon  the  left  side  of  the  chest  than  upon  the  right.  The  lower 
border  and  the  apex  impulse  are  not  defined,  as  the  heart  in 
this  situation  dipped  into  the  fluid  effusion  in  the  lower  recesses 
of  the  sac. 

REFERENCES. 

James:  American  Medicine,  1904,  vol.  viii.,  p.  23. 

LjtnsTGDAHL:  Deutsch.  Arch.  f.  klin.  Med.     Leipzig,  1913,  vol.cxi.,  p.  19. 

Wenckebach:  Zeitschr.  f.  klin.  Med.     Berlin,  1910,  vol.  Isxi.,  p.  402. 


CHAPTER  XXIX 
THE  TREATMENT  OF  PERICARDITIS 

The  treatment  of  acute  pericarditis  must  be  conducted  on 
lines  similar  to  those  which  have  been  considered  with  reference 
to  acute  endocarditis  (Chapter  XX.). 

The  essential  feature  is  absolute  rest,  both  bodily  and  mental, 
so  as  to  insure  the  minimal  amount  of  cardiac  strain,  and 
a  comfortable  bed-rest  is  often  required  for  patients  who  are 
unable  to  lie  flat  in  bed.  The  restriction  of  active  movements 
should  be  maintained  until  all  the  symptoms  have  disappeared, 
the  pulse-rate  has  returned  to  normal,  and  the  area  of  cardiac 
dulness  has  reverted  to  its  usual  limits .  The  patient  may  then 
be  allowed  to  move  about  in  bed,  but  he  should  not  be  allowed 
out  of  it  for  at  least  two  months  longer ;  and  for  another  month 
should  be  confined  to  a  couch.  Restrictions  as  to  exercise 
must  be  continued  for  three  to  six  months  afterwards,  and 
violent  exercise  prohibited  for  a  j^ear  longer. 

It  has  been  suggested  that  physical  exertion  should  be 
instituted  early  in  cases  of  pericarditis,  in  order  to  augment 
the  movements  of  the  heart,  and  so  limit  the  area  of  adhesion ; 
but  if,  as  I  believe  is  the  case,  one  of  the  main  functions  of  the 
pericardium  is  to  prevent  undue  distension  of  the  heart  during 
physical  exertion,  early  activity  is  likely  to  distend  the  inflamed 
sac  and  so  prevent  it  from  exercising  this  particular  function. 
It  is  not  uncommon,  too,  to  see  the  right  heart  dilate  tem- 
porarily^ from  even  trivial  exertion  early  in  convalescence,  and 
the  patients  in  whom  the  period  of  rest  has  been  prolonged 
have  always  seemed  to  me  to  have  smaller  hearts  than  those 
in  whom  physical  exertion  has  been  rapidly  resumed.  Adhe- 
sion of  the  visceral  and  parietal  layers  seems  to  interfere  little 
with  the  cardiac  action,  unless  mediastinitis  co-exists  and  the 

426 


THE  TREATMENT  OF  PERICARDITIS  427 

heart  is  fixed  to  the  chest  wall,  or  the  pericardial  sac  is  unduly 
large. 

Pain  when  present  must  be  relieved,  in  particular  in  those 
cases  in  which  it  interferes  with  sleep.  Local  applications, 
either  hot  or  cold  (an  ice  poultice  is  generally  comforting)  or 
sedative  applications,  such  as  glycerine  of  belladonna,  may  be 
sufficient;  leeches  or  blisters  are  sometimes  successful;  but 
opium  is  often  needed.  Pulv.  ipecac,  co.  or  a  hypodermic 
injection  of  morphia  is  generally  useful. 

In  many  cases  no  particular  line  of  treatment  is  indicated 
beyond  that  instituted  on  account  of  the  causal  condition.  In 
acute  rheumatism  salicylate  treatment  should  be  continued, 
but  large  doses  (above  120  grains  per  diem)  should  be  avoided. 
In  cases  where  cardiac  failure  is  impending  stimulants  may 
be  required.  Ammonia,  nux  vomica,  and  alcohol  have  seemed 
to  me  to  be  of  special  value  in  addition  to  drugs  of  the  digitalis 
group. 

In  cases  with  effusion  the  question  of  performing  para- 
centesis pericardii  naturall}"  arises,  but  the  general  impression 
that  it  is  rareh^  required  is  probably  correct,  as  death  is  seldom 
solely  due  to  the  pressure  exercised  upon  the  heart.  The 
results  of  operation,  too,  are  by  no  means  favourable.  In  West's 
series  33  out  of  67  cases  died,  including  4  out  of  11  rheumatic 
cases;  and  in  Delorme  and  Mignon's  series  65  per  cent,  of  82 
cases  proved  fatal.  The  results  of  incision  and  drainage  are 
also  unfavourable,  though  in  a  few  cases  recovery  has  ensued 
in  apparently  moribund  patients.  In  my  series  no  operation 
was  performed,  though  in  one  case  it  seemed  desirable.  The 
patient  was  the  boy  from  whom  the  skiagram  (Fig.  189)  was 
obtained,  and  the  pericarditis,  which  was  sero-fibrinous,  was 
secondary  to  a  septic  broncho-pneumonia,  accompanied  by 
left  pneumothorax.  Paracentesis  seemed  impossible,  and  the 
boy's  general  condition  from  the  pulmonary  aspect  negatived 
operative  interference  of  a  more  extensive  kind.  In  another 
case  post-mortem  examination  indicated  the  desirability  of  the 
operation.  The  apex  of  the  heart  was,  however,  firmly  ad- 
herent to  the  parietal  pericardium  and  to  the  chest  wall,  and 
had  remained  immobile  and  well  marked  during  the  whole 
progress  of  the  attack,  so  that  the  degree  of  the  effusion  was  not 


428  DISEASES  OF  THE  HEART 

estimated  correctly,  tlie  main  factor  in  the  increase  of  the  area 
of  cardiac  duhiess  being  ascribed  to  dilatation.  Six  of  the  30 
cases  recovered;  but  in  none  of  the  remaining  22  did  the  peri- 
carditis appear  chiefl}^  responsible  for  the  fatal  issue. 

In  purulent  pericarditis  incision  and  drainage  seem  indicated. 
I  have  never  seen  a  case  either  during  life  or  on  the  post-mortem 
table. 

Many  sites  have  been  suggested  for  the  operation,  but  the 
most  suitable  seems  that  suggested  by  Baizeau  and  Delorme 
and  Mignon — namely,  puncture  as  near  as  is  possible  to  the 
sternal  margin  in  the  fifth  or  sixth  left  intercostal  space.  The 
internal  mammarj^  vessels  and  the  left  pleural  cavity  are  thus 
avoided.  The  presence  of  friction  at  this  point,  or  loud  cardiac 
sounds  showing  that  the  heart  is  immediately  underneath, 
contra-indicate  this  site,  and  puncture  may  then  be  performed 
from  below  upwards  through  the  left  costo-sternal  angle,  or 
just  inside  the  left  border  of  dulness  and  outside  the  cardiac 
impulse.  The  pleural  cavity  is  necessarily  opened  in  the 
latter  case. 

The  treatment  of  cases  of  adherent  pericardium  in  which 
symptoms  of  cardiac  insufficiency  are  present  must  be  con- 
ducted upon  lines  similar  to  those  which  are  of  value  in  chronic 
valvular  disease.  Fibrolysin  has  been  recommended  in  those 
cases  with  a  view  to  the  dissolution  of  the  adhesions,  but  there 
are  no  records  of  siiry  very  notable  success.  In  one  of  my 
cases  the  patient  seemed  slightly  better  after  its  use. 

Operative  treatment  has  been  advocated  in  those  cases  of 
adherent  pericardium  where  the  heart  is  firmly  fixed  to  the 
thoracic  wall,  resection  of  those  portions  of  the  ribs,  costal 
cartilages,  or  sternum  which  are  involved  relieving  the  heart, 
from  much  unnecessary  work.  A  widespread  and  forcible 
movement  of  the  bony  and  cartilaginous  chest  wall  is  the 
special  indication  for  the  operation.  In  many  cases  of  ad- 
herent pericardium,  however,  the  cardiac  difficulties  arise  in 
other  ways  from  adhesion  to  the  diaphragm,  lungs,  or  medias- 
tinum, or  from  cicatricial  bands  around  the  heart  or  the  great 
vessels ;  and  suitable  cases  for  operation  are  by  no  means  fre- 
quently seen.  The  dangers  of  the  operation  are  considerable, 
sudden  death  on  the  operating-table  (which  occurred  in  the  only 


THE  TREATMEXT  OF  PERICARDITIS  429 

case  witli  which  I  have  been  personally  concerned)  being  nat 
infrequent,  and  pleurisy  often  succeeds,  as  the  pleural  cavity  is 
almost  necessarily  opened  during  the  operation.  I  believe, 
however,  that  a  more  careful  selection  of  cases  and  an  earlier 
operation  than  has  hitherto  been  carried  out,  will  in  the  future 
lead  to  better  results. 

A  similar  operation  has  been  suggested  in  cases  of  cardiac 
disease  accompanied  bj*  much  enlargement  of  the  heart  in  adrdt 
patients.  The  contour  of  the  chest  wall  is  rarely  deformed 
in  adults  by  cardiac  hj-pertroplw,  as  the  rib  arches  are  un- 
yielding, and  the  increased  space  within  the  thorax  demanded 
hj  the  heart  can  only  be  supplied  by  depression  of  the  dia- 
phragm and  lessening  of  the  pulmonary-  area.  The  removal  of 
portions  of  the  ribs  permits  enlargement  of  the  heart  forwards 
and  so  increases  the  pulmonary  area.  The  results  which  have 
been  obtained  are  at  anj^  rate  encouraging, 

REFERENCES  TO  C'ARDIOLYSIS. 

H.  T.  Bewley:  Brit.  Med.  Jom-n.,  1910,  vol.  i.,  p.  914. 
A.  Morison:  Lancet,  1908,  vol.  ii.,  p.  7.  (Literature.) 
W.  Thoeburx;  Brit.  Med.  Journ..  1910,  vol.  i.,  p.  10. 


INDEX 


Adherent  pericardium,  403 
Adrenalin  and  arterio-sclerosis,  40 
Alcohol  in  chronic  cardiac  failure,  384 

in  arterio-sclerosis,  92 
Alcoholism  and  arterio-sclerosis,  78 
Ammonium  salts  in  arterio-sclerosis,  84 
Aneurism  and  arterio-sclerosis,  56,  90 
blood-pressure  and,  90 
infective,  in  acute  endocarditis,  254 
of  heart,  28,  317 
sjrphilis  and,  277 
Anginal  pain,  289 
Ante-mortem  clots,  306 
Aorta,  rupture  of,  267 
syphilis  of,  43,  267 
Aortic   valvular   disease,   acute   endo- 
carditis and,  276 
arterial  disease  and,  274, 

278 
blood-pressure  in,  90,  298 
cardiac  rhythm   in,   285, 

364 
causes   of   symptoms   in, 

282 
Cheyne-Stokes    breathing 

m,  287 
chorea  and,  276 
comparison    with    mitral 

disease,  302 
coronary  arteries  ua,  265 
cough  in,  288 
diagnosis  of,  346,  349 
dyspnoea  in,  303 
etiology,  275 
Flint's  murmur  in,  351 
general    cardio  -  vascular 
degeneration  and,  278 
incidence  of,  275 
left  ventricle  in,  299 
mechanical     strain     and, 

277 
mitral  incompetence  and, 

301 
morbid  anatomy  of,  261 
murmurs  in,  297 
myocardial  failure  m,  284 
onset  of  symptoms  in,  301 
oedema  in,  291 


Aortic  valvular  disease,  pain  in,  289 
palpitation  in,  289 
prognosis  in,  348,  351 
pulse  in,  348,  351 
renal    disease    and,    272, 

277,  301 
symptoms  of,  282,  297 
syphilis  and,  277 
treatment  of,  370 
Aortic  valves,  mechanism  of  the,  297 
Apex  tracings,  106,  323 

the  a  wave  in,  108 
inverted,  323 
Arterial  diseases,  30 

arterio-sclerosis  (q.v.) 
atheroma,  41 

Bright's  disease  and,  57,  65 
calcareous  degeneration,  47 
diffuse  lesions,  32 
endarteritis  obliterans,  44 
focal  lesions,  41 
mesarteritis,  43 
symptoms  of,  54 
syphilitic,  43 
Arteries,  retinal,  72 
structure  of,  30 
vascular  arrangements  of,  31 
Arterio-sclerosis,  32 
adrenalin  and,  40 
albuminuria  in,  65 
alcoholism  and,  78 
and  aneurism,  56,  90 
and  cardiac  hypertrophy,  61 
apex  impulse  in,  64 
blood-pressure  in,  36,  57,  68,  82 
bronchitis  in,  77 
cardiac  failure  in,  65,  78,  81 
constipation  in,  93 
diagnosis  of,  60,  63 
diet  and,  92,  95 
diuretics  and,  93 
drugs  in,  96 
elastic  fibres  in,  33 
emphysema  in,  70 
enteric  fever  and,  40 
etiology  of,  36 
exercise  and,  93 
haemorrhage  in,  79 


431 


432 


DISEASES  OF  THE  HEART 


Arterio-sclerosis.  heart-sounds  in,  65 
iodine  in,  97 
lead-poisoning  and,  40 
massage  in,  95 

miliary  aneurisms  and.  54.  74 
morbid  anatomy,  32 
ocular  manifestations  in.  72 
oral  sepsis  in,  94 
polycythsemia  and,  37 
purgatives  in,  87,  93 
renal  changes  in,  36,  56,  57,  65 
repletion  and.  39 
sepsis  and,  79 
shortness  of  loreath  in,  70 
symptoms  of.  54 
treatment,  75 
uraemia  in,  69,  87 
valvular  flaws  in,  66 
vaso-dilator  drugs  in,  84,  96 
visceral  lesions  in,  56 
viscosity  of  the  blood  in,  36 
Ascites  in  adherent  pericardium,  405 
Atheroma,  41 
Atrophy  of  the  heart-muscle,  7 

ischsemic,  S 
Auricles,  arrangement  of  musculature 

of,  1 
Auricular  fibrillation,  211 

arterial  pulse  in,  212 

auricular  muscle  in,  216 

cervical  curve  in,  212 

digitalis  in,  219 

duration  of,  214 

electro -cardiogram  in,  122,  213 

etiology  of,  215 

experimental    production    of, 
211 

infarcts  in,  218 

mitral  stenosis  and,  215 

murmurs  in,  218 

presystolic  murmui  in,  217 

prognosis  in,  218 

stimulus  production  in.  213 

symptoms  of,  214 

treatment  of,  219 
Auricular  flutter,  198 

arterial  curve  in,  202 

aortic  disease  and,  209 

auricular  contractions  and,  200 

cervical  curve  in,  199 

digitalis  in,  210 

electro-cardiogram  of,  199 

etiology  of,  195 

incidence  of,  209 

mitral  disease  and,  209 

paroxysmal  tachycardia  and, 
209 

prognosis  in,  209 

symptoms  of,  203 

treatment  of,  210 

ventricular     contractions     in. 
200 


Auriculo-ventricular  bundle.  101 

the  relations  of,  151 

branches  of,  102 
Auriculo-ventricular  node,  the.  101 

the  relations  of,  151 
Aiu"iculo-ventricular  valves,  mechanism 
of  the,  294 

Baillie's  pill,  383 

Blood-cultures   m   acute   endocarditis. 
233,  251,  258 

Blood-pressure  in  aneurism.  90 
in  aortic  reflux,  90,  299 
in  aortic  stenosis,  67,  299 
in  arterio-sclerosis,  68,  82 
in  mitral  disease,  66,  90,  295 
in  paroxysmal  tachycardia,  188 

Broadbent's  sign,  407 

Bronchitis  in  mitral  disease,  303 

Bruit  de  Boger,  357 

Caffeine  in  arterio-sclerosis,  84 

in  chronic  valvular  disease,  384 
Cardiac  failure,  causes  of,  282 

treatment  of,  370 
Cardiolysis,  428 
Carditis,  rheiunatic,  20 

and  endocarditis,  150 
Cervical  curve,  106 

the  a  wave  in,  109 
the  a-c  interval  in,  112 
the  c  wave  in,  108 
the  /i  wave  in,  113 
the  V  wave  in,  110 
the  .T  depression  in.  111 
the  y  depression  in.  Ill 
Cheyne-Stokes  respiration,   in   arterial 
disease,  71 
in  valvular  disease,  287 
Chordae    tendinese,    in   acute    endocar- 
ditis, 222 
in  mitral  disease,  264 
Chorea  and  acute  endocarditis,  228 

and  chronic  valvular  disease.  20G. 

276 
and  pericarditis,  389 
Cloudy  swelling  of  myocardium,  9 
Coagulation  necrosis,  hyaline  degenera- 
tion and,  9 
Conductivity,    162.       Cf.    also    Heart - 
block 
asphyxia  and,  162 
atropine  and,  163 
digitalis  and,  162 
murmurs  in  defective,  166 
swallowuig  and,  162 
vagus  stimulation  and,  162 
Congenital    heart  disease  and  chronic 
valvular  disease,  274 
and    malignant    endocai  - 

ditis,  230 
diagnosis  of,  356 


INDEX 


433 


Connective  tissue  of  the  heart,  2 

in  cardiac  hypertrophy,  8 
Contractility,  159 

prognosis  in  defective,  161 
pulsus  alternans  and,  161 
Convallaria,  384 
Coronary  arteries,  the,  2 

anastomosis  of.  3 

circulation  of,  2 

closure  of,  5 

in  aortic  incompetence.  265 

ligature  of,  6 

supplementary,  3 

variations  in  origin  of,  4 
Coupled  rhythms,  175 

auricular  fibrillation  and,  176 

digitalis  and,  380 

etiology  of,  176 

extra-systoles  and,  175 

partial  heart-block  and,  175 

Death,  sudden,  363 

Derivation  L,  115 

Derivation  II.,  115 

Derivation  III.,  115 

Diastole,  cardiac,  110 

Digitalis,  376 

in  aortic  incompetence,  383 

in  arterio-sclerosis,  84,  378 

iu  auricular  fibrillation,  219,  381 

in  auricular  flutter,  210,  381 

in  chronic  cardiac  failure,  380 

dangers  of,  380 

in  heart-block,  381 

ia  paroxysmal  tachycardia,  381 

Dissociation,  10 

Diuretin,  iu  arterio-sclerosis,  84 
LQ  chronic  cardiac  failure,  384 

Ductus  arteriosus,  patent,  357 

Duroziez's  sign  in  aortic  incompetence, 
351 

Dysphagia  in  acute  pericarditis,  393 

Dyspnoea,    in   chronic   cardiac  failure, 
286 
in  pericarditis,  394 

Effusion,  pericardial,  characters  of,  386 
diagnosis  of,  399 
symptoms  of,  392 
treatment  of,  426 
Electro -cardiogram  of  auricular  fibrilla- 
tion, 122 
in  extra -systoles,  120 
in  aortic  incompetence,  119 
in  heart-block,  119 
in  heart-failure,  118 
in  mitral  stenosis,  118 
normal,  116 
of  auricular  flutter,  122 
Electro-cardiograph,  the,  114 
Embolism.  290,  306.  308,  314 
cardiac,  16 


Embolism,  cerebral,  293,  308 

in  acute  endocarditis,  246,  254 
in  mitral  stenosis,  295,  306 
pulmonary,  303 
renal,  254,  306 

Emphysema  and  arterio-sclerosis,  70 

Endarteritis  deformans.  41 
etiology  of,  50 

Endarteritis  obliterans.  44 
etiology  of,  50 

Endocarditis,  acute,  220 
aortitis  in,  223 
aneurism,    infective,    in,    224, 

254 
auscultatorv  evidence  of,  237 
blood-cultures  in,  230,  258 
cardiac  muscle  in,  226 
cardiac  overaction  in,  236 
chorea  and,  228 
cutaneous    manifestations    ot, 

255 
diagnosis  of,  251 
embolism  in,  254 
enteric  fever,  228 
etiology  of,  227 
extra-svstoles  in,  236 
fever  in,  238,  251 
heart-block  in,  236,  245 
hemiplegia  in,  246 
incidence  of,  227 
influenza  and,  228,  233 
leucocytosis  in,  255 
local  infectious  and,  229 
massage  in,  257 
micro-organisms  in,  221,  230 
morbid  anatomy  of,  220 
mural,  223 
murmurs  in,  237,  254 
nodal  rhji}hm  in,  236,  242 
pericarditis  and,  227,  237 
pneumonia  and,  228 
Xjrognosis  of,  255 
puLse  in,  235,  253 
rest  in,  256 

rheumatism  and,  227,  231,  257 
scarlatina  and,  228 
septic  foci  in,  259 
symptoms  of,  234 
subcutaneous  nodules  in,  237 
tonsillitis  and,  228 
treatment  of,  255 
valves  affected  in,  232 

Endocarditis,    chronic.       C/.    Valvular 
disease,  chronic 

Endocarditis,  malignant,  229 
blood-cultures  in,  233 
I  childbirth  and,  230 

diagnosis  of,  251 
exanthemata  and,  229 
incidence  of,  229,  232 
micro-organisms  in,  230 
morbid  anatomy  of,  222 
28 


434 


DISEASES  OF  THE  HEART 


Endocarditis,   malignant,  predisposing 
causes  of,  232 
rheumatism  and,  229 
site  of  lesions  in.  232 
symptoms  of,  234 
treatment  of,  257 
Enteric  fever  and  arterio-sclerosis,  40 
and  acute  endocarditis,  228 
Epigastric  pulsation,  323 
Epileptic  convulsions  and  bradycardia, 

166 
Excitability,  125 
Extra  systoles,  125 
auricular,  127 
causes  of,  129 
in  acute  endocarditis,  236 
in  alcoholic  poisonuig,  131 
in  aortic  disease.  363 
m  fevers,  131,  332 
in  mitral  disease,  363 
in  nicotme  poisonuig,  131 
interpolated,  125 
nodal,  127 
prognosis,  132 
symptoms,  132 
treatment,  132 
ventricular,  125 

Fatty  degeneration  of  the  heart,  1 1 
causes  of,  14 
diffuse,  14 
distribution  of,  12 
frequency  of,  11 
patchy,  14 
Fattj'  infiltration  of  the  heart,  10 

obesity  and,  11 
Fibrosis,  arterio-capillary,  32 
Fibrosis  of  heart,  15 

and  coronary  disease,  24,  26 
distribution  of,  16 
gummata  in,  26 
haemorrhages  in,  26 
hydatid  cj^sts  in,  26 
mixed  form,  24 
para-arterial,  17 
causes  of,  19 
peri-arterial,  19 

causes  of,  20 
syphilis  in,  26 
trauma  in,  26 
tumours  in,  26 
Fhst-rib  sign,  the,  in  pericardial  effu- 
sion, 400 
Flint's  murmur,  351 
Focal  lesions  of  arteries.  41 
etiology  of,  48 
Foramina  Thebesii,  6 
Fragmentation  of  cardiac  muscle,  10 
Friction-sounds   in  acute   pericarditis, 

397 
Fimdus  oculi,  the,  in  arterio-sclerosis, 
72 


Granular    degeneration    of    the    myo- 

cardirun.  9 
Gumma  of  the  heart,  26 

and  heart-block,  170 
Guy's  pill,  383 

H  wave,  113 

H  asmopericardium ,  396 

Haemoptysis  ui  mitral  stenosis,  288 

in  pulmonary  embolism,  288 
Heart,  congenital  diseases  of  the,  356 
patent  ductus  arteriosus, 

357 
septal  defects,  357 
Heart,  aneurism  of,  28,  317 

contraction  of,  98 

fatty  degeneration  of,  11 

fatty  infiltration  of,  10 

fibroid  disease  of,  15 

in  adherent  pericardium,  406 

in  aortic  disease,  297 

in  arterio-sclerosis,  60 

in  mitral  disease,  294 

mobility  of,  320 

reserve  power  of,  283 

wounds  of,  26 
Beart-block,  acute,  170,  172 

and  Stokes-Adams  syndrome,  166 

auricular  contractions  in,  171 

chronic,  165 

full,  163 

in  acute  endocarditis,  236,  245 

m  the  acute  infections,  172 

morbid  anatomy  of,  170 

partial,  164 

prognosis  in,  172 

sjTnptoms  of,  165 

treatment  of,  173 
Heart-failure,  282 

and  high  blood-pressure,  62 
Heart,  rupture  of,  28 
Hemiplegia,  in  acute  endocarditis,  247 

in  aortic  disease,  308 

in  mitral  disease,  308 
Hyaline  degeneration,  9 
Hypermyotrophy,  35 
Hyperpiesis,  39 
Hypertrophy  of  heart,  7 
Hypnotics  in  chronic  cardiac  failure,  375 

Infections,  acute,  and  acute  endocar- 
ditis, 228 
and  pericarditis,  390 
Influenza  and  acute  endocarditis,  228 
Intermittent  claudication  and  arterio- 
sclerosis, 71 
Intestine,  infarction  of  the,  290 
Iodine  in  arterio-sclerosis,  97 

Jaundice  and  bradycardia,  124 

in  mitral  stenosis,  362 
Jugular  veins,  109 


INDEX 


435 


Leucocytosis  in  acute  endocarditis,  255 
Liver,  the,  in  mitral  disease,  290 

in  tricuspid  reflux,  356 
Lungs,   the,   hsemorrhagic   infarcts   of, 
288,  303 

in  aortic  disease,  302 

in  mitral  disease,  303 

Massage  iu  acute  endocarditis,  257 
in  chronic  cardiac  failure,  371 
Medial  calcification,  47 
Mediastinitis,  chronic,  403 
Mediastino-pericarditis,  403 
Medulla,   disease  of   the,   and   Stokes- 
Adams  disease,  170 
Mesarteritis,  patchy,  43 
Miliary  aneurisms   in   arterio-sclerosis, 

54,  74 
Milk  diet  in  arterio-sclerosis,  92 

in  chronic  cardiac  failure,  374 
ililk-spots,  pericardial,  387 
Mitral  incompetence,  332 
diagnosis.  342 
etiology,  362 
murmurs  of,  342 
prognosis,  363 
Mitral  stenosis,  332 

diagnosis,  333 
murmurs  of,  335 
prognosis,  363 
Mitra]  valvular  disease,  acute  endocar- 
ditis and,  277 
blood-pressure     in,     295, 

341 
cardiac  rhythm  in,  285 
causes  of,  275 
causes  of  symptoms,  282 
cerebral  symptoms  in,  293 
Cheyne-Stokes    breathing 

in,  287 
chorea  and,  277 
comparison    with    aortic 

disease,  302 
cough  in,  288 
dyspnoea  in,  286 
embolism  in,  293 
gastro  -  intestinal    symp- 
toms in,  292 
general     cardio  -  vascular 
degeneration  and,  278 
haemoptysis  in,  288 
incidence  of,  279,  280 
in  women,  280 
mechanical     strain     and, 

277 
morbid  anatomy  of,  261 
murmurs  in,  295 
oedema  in,  291 
onset  of  symptoms  in,  296 
pain  in,  289 
palpitation  in,  289 
renal  disease  and,  269 


Mitral    valvular    disease,   rheumatism 
and,  277 
symptoms  of,  294 
syphilis  and,  277 

Murmurs,  328 

cardio-pulmonary,  330 

conduction  of,  326 

in  acute  endocarditis,  237,  254 

in  aortic  incompetence,  349,  350 

in  aortic  stenosis,  348 

in  mitral  incompetence,  295,  344 

in  mitral  stenosis,  337,  340 

in  patent  ductus  arteriosus,  358 

in  pulmonary  incompetence,  355 

in  pulmonary  stenosis,  355 

in  tricuspid  incompetence,  357 

in  tricuspid  stenosis,  357 

presystolic,  337 

Myocarditis,  19 

Myocardium,  disease  of  the,  1 

and  acute  infections,  309 

Myocardium,  the,  atrophy  of.  7 
cloudy  swelling  of,  9 
coronary  arteries  and,  312 
failure  of,  309 

fatty  degeneration  of,  11,  311 
fatty  infiltration  of,  10.  311 
fibrosis  of,  315 
granular  degeneration  of,  9 
hyaline  degeneration  of,  9 
hypertrophy  of,  7 
infarction  of,  16 
ischsemic  atrophy  of,  8 
para-arterial  fibrosis  of,  17 
peri-arterial  fibrosis  of ,  19 
rheumatic  nodules  in,  21 
rheumatism  and,  150 

Myogenic  theory,  the,  98 

Myomalacia  cordis,  16 

Nativelle's  digitalin,  383 

Nerve,    recurrent    laryngeal,    the,    in 

mitral  obstruction,  288 
Nervous  system  and  functions  of  the 

heart,  105 
Nodal  rhythm,  133 

cardiac  weakness  in,  148 
in  acute  endocarditis,  236,  242 
the  a.-v.  node  in,  148 
the  a.-v.  bundle  in,  148 
the  pulse  in,  148 
Node,  auriculo-ventricular,  101 

sino-auricular,  100 
Nodules,  subcutaneous,  21 

Qildema  in  aortic  disease.  291.  305    ■ 
in  mitral  disease,  291,  305 
in  tricuspid  incompetence,  356 

CEsophagus,    the,    obstruction    of,    ia 
pericarditis,  395 
trauma  of,  and  pericarditis,  418 


436 


DISEASES  OF  THE  HEART 


P  deflection.  116 
Palpitation,  289 
Paracentesis  pericardii,  428 
Paroxj-smal  tachycardia,  184 

auricular  flutter  and,  194 

cardiac  reserve  in,  188 

cervical  curve  in,  192 

dilatation  of  heart  in,  197 

electro -cardiogram  in,  193 

etiology  of,  195 

incidence  of,  196 

nodal  form,  184 

prognosis  in,  196 

pulse-rate  in,  188 

stimulus  production  in,  194 

symptoms  of,  184 

treatment  of,  196 
Pericarditis,  acute,  385 

acute  rheumatism  and,  388 

chorea  and,  389 

diagnosis  of,  397 

effusion  in,  399 

etiology  of,  388 

incidence  of,  385 

milk-spots  and,  387 

morbid  anatomy,  385 

onset  of,  393 

paracentesis  in,  428 

prognosis  in,  402 

pulse  in,  394 

pyaemia  and,  390 

renal  disease  and,  390 

symptoms  of,  391 

terminal,  390 

the  infections  and,  390 

thoracic  disease  and,  390 

treatment,  426 
X-ray  examination  in,  401 
Pericardium,  adherent,  403 

Broadbent's  sign  in,  407 

cardiolysis  in,  428 

chronic  mediastinitis,  403 

diagnosis  of,  406 

etiology  of,  404 

indurative  mediastino-pericar- 

ditis,  403 
mediastino-pericarditis,  403 
morbid  anatomy,  403 
pericarditis  interna  et  externa, 

403 
Pick's  disease,  405 
pulsus  paradoxus  in,  409 
symptoms  of,  404 
treatment  of,  428 
Petit  mal  and  Stokes-Adams  disease, 

166 
Physical  signs,  in  aortic  incompetence, 
349 
in  aortic  stenosis,  346 
in  mitral  incompetence,  342 
in  mitral  stenosis,  333 
in  myocardial  failure,  331 


Physical   signs,   in  pulmonary  incom- 
petence, 354 
in  pulmonary  stenosis,  353 
in  tricuspid  incompetence,  354 
in  tricuspid  stenosis,  356 
of  adberent  pericardium,  406 
of  fibrinous  pericarditis,  397 
of  pericardial  effusion,  399 
of  pneumo -pericardium,  419 
significance  of,  320 
Pick's  disease,  405 
Pneumonia  and  acute  endocarditis,  228 

and  pericarditis,  390 
Pneumo -pericardium,  418 
diagnosis  of,  419 
etiology,  418 
prognosis,  419 
symptoms,  419 
treatment  of,  419 
Polycythsemia,  37 

Polygraph  curves,  interpretation  of,  106 
Polyorrhomenitis,  or  polyserositis,  405 
Presphygmic  interval,  128 
Primitive  cardiac  tissue,  the,  99 
Prognosis,  361 
age  and,  368 
cause  of  failure  and,  367 
degree  of  compensation  and,  366 
disease  of  other  viscera  and,  366 
embolism  and,  361 
grade  of  the  lesion  and,  364 
jaundice  and,  362 
nature  of  lesion  and,  362 
rhythm  of  the  heart  and,  364 
sex  and,  369 
site  of  lesion  and,  363 
social  conditions  and,  369 
Prognosis  in  acute  endocarditis,  255 
in  aiu^icular  fibrillation,  218 
in  auricular  flutter,  209 
in  coupled  rhythms,  183 
in  chronic  cardiac  failure,  361 
in  dilatation  of  the  heart,  345,  353 
in  extra-systoles,  132 
in  heart-block,  172 
in  infantile  irregularity,  124 
in  paroxysmal  tachycardia,  196 
in  pericarditis,  402 
in  pneumo-pericardium,  419 
in  pulsus  alternans,  161 
Pulmonary  incompetence,  354 
due  to  dilatation,  353 
mitral  stenosis  and,  339 
Pulmonary  stenosis,  353 
Pulsation,  prsecordial,  323 
Pulse,  the,  alternation  of,  153 

in  acute  endocarditis,  235,  253 

in  aortic  incompetence,  351 

in  aortic  stenosis,  347 

in  Cheyne-Stokes  breathing,  124 

in  heart-block,  1G5 

in  mitral  disease,  66,  340 


INDEX 


437 


Pulse,  the,  in  paroxysmal  tachycardia, 
188 
in  the  Stokes-Adams  syndrome,  169 
palpation  of,  60 
pressure  of,  60 

respiratory  irregularity  of,  123 
Pulsus  alternans,  161 
bigeminus,  180,  183 
paradoxus,  409 

in  adherent  pericardium,  409 
Purgatives  in  chronic  cardiac  failure, 

378 
Purkinje  fibres,  103 
Pyopericardium.  396 

Q  deflection,  117 

R  deflection,  117 

Renal  disease  and  aortic  disease,  272, 
277,  301 
and  arterio-sclerosis,  36,  56,  65 
and  high  blood-pressure,  36 
and  mitral  disease,  66,  271,  301 
and  pericarditis,  390 
Retinal  vessels,  72 
Rheumatic  nodules  in  myocardium,  21, 

150 
Rheumatism    and    acute    endocarditis, 
227,  231,  257 
and  aortic  disease,  276 
and  disease  of  the  right  side  of  the 

heart,  353 
and  mitral  disease,  277 
and  pericarditis,  388 
and  Stokes-Adams  syndrome,  172 
Rhythm,  nodal,  of  the  heart,  133 

coupled,  175 
Rupture  of  heart,  28 

S  deflection,  116 

Salicylates,  the,  in  acute  endocarditis, 
258 
in  acute  pericarditis,  427 
Scarlet  fever   and  acute    endocarditis, 
228 
and  pericarditis,  390 
Segmentation  of  cardiac  muscle,  10 
Semilunar   valves,   the  mechanism   of, 

297 
Septum,  congenital  defects  of  the  car- 
diac, 357 
Sign,  Broadbent's,  407 

Duroziez's,  351 
Sino -auricular  node,  the,  100 
Sounds  of  the  heart,  the  reduplication 

of,  339 
Stenosis,  aortic,  346 
mitral,  333 
pulmonary,  353 
tricuspid,  356 
Stimulus  production,  123 
Stokes-Adams  syndrome,  166 


String  galvanometer,  114 

Strophanthus  in  chronic  valvular  dis- 
ease, 383 

Strychnine  in  chronic  valvular  disease, 
384 

Subcutaneous  nodules  in  acute  endo- 
carditis, 149,  237 

Syphilis  and  aortic  disease,  277 
and  arterial  degeneration,  43 
and  chronic  valvular  disease,  267 
and  mitral  disease,  277 

Symptoms  of  acute  endocarditis,  234 
of  adherent  pericardium,  404 
of  aortic  disease,  282,  297 
of  arterial  disease,  54 
of  auricular  fibrillation,  214 
of  auricular  flutter,  203 
of  chronic  cardiac  failure,  282 
of  mitral  disease,  294 
of  myocardial  failure  in  myocardial 

disease,  311 
of  myocardial  failure  in  the  infec- 
tions, 309 
of  paroxysmal  tachycardia,  184 
of  pericarditis,  391 
of  pneumo-pericardium,  410 

T  deflection,  116 
Tachycardia,  paroxysmal,  184 
Theobromine,  84,  384 
Thoracostomy     in     chronic     valvular 
disease,  429 
in  pericardial  adhesions,  428 
Thrombosis  in  auricles,  306 

in  focal  lesions  of  the  arteries,  55 
Tonicity,  174 

Tonsillitis  and  acute  endocarditis,  228 
Treatment  of  acute  endocarditis,  255 
of  adherent  pericardium,  428 
of  arterio-sclerosis,  75 
of  auricular  fibrillation,  219 
of  auricular  flutter,  210 
of  extra-systoles,  132 
of  heart-block,  173 
of  paroxysmal  tachycardia,  196 
of  pericarditis,  426 
Treatment  of    chronic  cardiac  failure, 
370 
alkalies  in,  378 
caffeine  in,  384 
diet  in,  371 
digitalis  in,  376 
mercury  in,  378 
of  symptoms,  374 
rest  in,  370 
squills,  383 
strophanthus,  383 
theobromine,  384 
Tricuspid  incompetence,  354 
stenosis,  356 

valves,  endocarditis  and,  352 
Tuberculosis  and  pericarditis,  396 


438 


DISEASES  OF  THE  HEART 


Undefended  space,  the,  151 
Uraemia  and  arterial  disease,  69,  87 
and  chronic  valvular  disease,  286 

Vaccines  in  acute  endocarditis,  258 
Valvular  disease,  chronic,  261 

acute    endocarditis    and 

266 
and  congenital  defects,  274 
and  general  cardio-vascu- 

lar  degeneration,  273 
cardiac  rhythm  in,  285 
Cheyne-Stokes    breathing 

•in,  287 
cough  in,  288 
diagnosis,  320 
dyspnoea  in,  286 
etiology  of,  266 
gastro-intestinal    disturb- 
ances in,  292 


Valvular  disease,   chronic,  mechanical 
strain  and,  267 
morbid  anatomy  of,  261 
myocardial  failure  in,  284 
oedema  in,  291 
pain  in,  289 
.     palpitation  in,  289 
prognosis  of,  361 
renal  disease  and,  269 
symptoms  of,  282 
syphilis  and,  267 
treatment  of,  370 
Vaso-dilator  drugs  in  arterio-sclcrosis, 

84,  96 
Ventricles,  arrangement  of  musculature 

of,  2 
Viscosity  of  the  blood,  the,  36 

X-ray  examination,  48.  334,  338,  401, 
417.  423,  424 


BILLING  AND  SONS,    LTD.,    PKINTKKS,    GUILDFORD 


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